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296 Cards in this Set
- Front
- Back
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Question
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Answer
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3-year-old boy presents with facial edema, malaise, and proteinuria.
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Steroids for minimal change disease.
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oman presents with UTI positive for Proteus vulgaris. What type of kidney stones is she at risk for?
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Ammonium magnesium phosphate (struvite).
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Patient describes a 2-year history of acetaminophen use. What is she at risk for?
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Renal papillary necrosis.
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X-ray film shows massively enlarged kidneys bilaterally.
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Adult polycystic kidney disease.
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Patient taking enalapril complains of constant coughing. Alternative
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Losartan—angiotensin II eceptor blocker.
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Ureters: course
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Ureters pass under uterine artery and under ductus Water (ureters) under the deferens (retroperitoneal). bridge (artery, ductus deferens).
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The ????? kidney is taken during transplantation because ????
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left has a longer renal vein.
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Ions in ECF vs ICF
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ECF: ↑ NaCl, ↓ K+ ICF: ↑ K+, ↓ NaCl
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ECF – PV =
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interstitial volume.
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TBW – ECF =
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ICF.
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60–40–20 rule (% of body weight):
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60% total body is water 40% ICF 20% ECF
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Plasma volume measured by? Extracellular volume measured by?
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radiolabeled albumin. inulin.
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plasma Osmolarity is approximately
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290 mOsm
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Renal clearance equation
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Cx= UxV/Px = volume of plasma from which the substance is completely cleared per unit time. Cx= clearance of X. Ux= urine conc of X. Px= plasma conc of X. V = urine flow rate.
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If Cx< GFR, If Cx> GFR, If Cx= GFR,
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-If Cx< GFR, then there is net tubular reabsorption of X -If Cx> GFR, then there is net tubular secretion of X. -If Cx= GFR, then there is no net secretion or reabsorption.
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Responsible for filtration of plasma according to size and net charge.
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Glomerular filtration barrier
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Glomerular filtration barrier is responsible for
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Responsible for filtration of plasma according to size and net charge.
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Glomerular filtration barrier is composed of
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1. Fenestrated capillary endothelium (size barrier) 2. Fused basement membrane with heparan sulfate (negative charge barrier) 3. Epithelial layer consisting of podocyte foot processes
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Glomerular filtration barrier what is lost in nephrotic syndrome and what does that lead to
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The charge barrier is lost in nephrotic syndrome, Resulting in: albuminuria, hypoproteinemia, generalized edema, and hyperlipidemia.
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When is the negative chare barrier lost on the Glomerular filtration barrier
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nephrotic syndrome,
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Glomerular filtration rate things used to measure
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Inulin or Creatinine
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Inulin can be used to calculate GFR because
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it is freely filtered and is neither reabsorbed nor secreted.
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Inulin GFR calculation
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GFR = Uinulin × V/Pinulin = Cinulin= Kf[(PGC – PBS) – (πGC – πBS)]. (GC = glomerular capillary; BS = Bowman’s space.) πBS normally equals zero.
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Effective renal plasma flow things used to measure
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PAH (para-Aminohippurate)
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Effective renal plasma flow calculation and blood flow
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ERPF = UPAH × V/PPAH = CPAH. RBF = RPF/1− Hct. ERPF underestimates true RPF by ~10%.
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ERPF can be estimated using PAH because
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ERPF can be estimated using PAH because it is both filtered and actively secreted in the proximal tubule. All PAH entering the kidney is excreted.
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Filtration fraction = GFR/RPF.
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GFR/RPF.
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GFR/RPF =
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Filtration fraction
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Filtered load =
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GFR × plasma concentration.
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GFR × plasma concentration =
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Filtered load
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Free water clearance describe and calculate
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Given urine flow rate, urine osmolarity, and plasma osmolarity, be able to calculate free water clearance: CH2O = V − Cosm. V = urine flow rate; Cosm = UosmV/Posm.
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Glucose clearance different levels wrt blood Glc
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-At plasma glucose of 200 mg/dL, glucosuria begins (threshold). -At 350 mg/dL, transport mechanism is saturated (Tm).
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Glucose clearance what hapens to Glc at normal levels
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Glucose at a normal plasma level is completely reabsorbed in proximal tubule.
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Amino acid clearance describe
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Reabsorption by at least 3 distinct carrier systems, with competitive inhibition within each group. 2° active transport occurs in proximal tubule and is saturable.
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Early proximal convoluted tubule what is resorbed and what is secreted
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Reabsorbs all of the glucose and amino acids and most of the bicarbonate, sodium, and water. Secretes ammonia, which acts as a buffer for secreted H+.
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“workhorse of the nephron.”
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A. Early proximal convoluted tubule
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Thin descending loop of Henle what is resorbed and what is secreted
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passively reabsorbs water via medullary hypertonicity (impermeable to sodium).
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Thick ascending loop of Henle what is resorbed and what is secreted
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actively reabsorbs Na+, K+, and Cl − and indirectly induces the reabsorption of Mg2+ and Ca2+. Impermeable to H2O.
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Early distal convoluted tubule what is resorbed and what is secreted
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actively reabsorbs Na+, Cl −. Reabsorption of Ca2+ is under the control of PTH.
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Collecting tubule what is resorbed and what is secreted
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reabsorb Na+ in exchange for secreting K+ or H+ (regulated by aldosterone). Reabsorption of water is regulated by ADH/vasopressin
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What part of the nephron is Reabsorbs all of the glucose and amino acids and most of the bicarbonate, sodium, and water. Secretes ammonia, which acts as a buffer for secreted H+.
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Early proximal convoluted tubule
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What part of the nephron is Reabsorbs most of the bicarbonate , sodium, and water.
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Early proximal convoluted tubule
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What part of the nephron is Secretes ammonia, which acts as a buffer for secreted H+.
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Early proximal convoluted tubule
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What part of the nephron is passively reabsorbs water via medullary hypertonicity (impermeable to sodium).
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Thin descending loop of Henle
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What part of the nephron is Impermeable to H2O.
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Thick ascending loop of Henle
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What part of the nephron is actively reabsorbs Na+ K+, and Cl and indirectly induces the reabsorption of Mg2+ and Ca2+.
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Thick ascending loop of Henle
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What part of the nephron is actively reabsorbs Na+, Cl- Reabsorption of Ca2+ is under the control of PTH.
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Early distal convoluted tubule—
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What part of the nephron is Reabsorption of Ca2+ is under the control of PTH.
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Early distal convoluted tubule
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What part of the nephron is reabsorb Na+ in exchange for secreting K+ or H+ (regulated by aldosterone).
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Collecting tubules
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What part of the nephron is reabsorption of water is regulated by ADH/vasopressin
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Collecting tubules
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Osmolarity of medulla can reach 1200 mOsm/L H2O.
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1200 mOsm/L H2O.
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Renin-angiotensin system Mechanism
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Renin is released by the kidneys upon sensing ↓ BP and cleaves angiotensinogen to angiotensin I. Angiotensin I is then cleaved by angiotensin-converting enzyme (ACE), primarily in the lung capillaries, to angiotensin II.
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Actions of angiotensin II
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1. Potent vasoconstriction 2. Release of aldosterone from the adrenal cortex 3. Release of ADH from posterior pituitary 4. Stimulates hypothalamus →↑ thirst
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Overall, angiotensin II serves to
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↑ intravascular volume and ↑ BP.
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??? released from atria may act as a “check” on the renin-angiotensin system (e.g., in heart failure). Decreases renin and increases GFR.
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ANP
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ANP as a check on renin-angiotensin
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ANP released from atria may act as a “check” on the renin-angiotensin system (e.g., in heart failure). Decreases renin and increases GFR.
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JG cells What type . JG cells secrete
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(modified smooth muscle of afferent arteriole)
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macula densa What does it sense and where is it
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(Na+ sensor, part of the distal convoluted tubule)
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JG cells secrete
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renin
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what cells secrete renin
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JG cells
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(Na+ sensor, part of the distal convoluted tubule)
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macula densa
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Juxtaglomerular apparatus (JGA) main purpose
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GA defends glomerular filtration rate via the renin- angiotensin system.
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Juxtaglomerular apparatus (JGA) components
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JG cells and macula densa
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Kidney endocrine functions in general
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epo Vit D Renin Protaglandins
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What causes JG cells to secrete renin
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↓ renal blood pressure, ↓ Na+ delivery to distal tubule, ↑ sympathetic tone (via β1)
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Kidney endocrine functions describe mech of EPO
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Endothelial cells of peritubular capillaries secrete erythropoietin in response to hypoxia
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Kidney endocrine functions describe mech of Vit D
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Conversion of 25-OH vitamin D to 1,25-(OH)2vitamin D by 1α-hydroxylase, which is activated by PTH
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Kidney endocrine functions describe mech of prostaglandins
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Secretion of prostaglandins that vasodilate the afferent arterioles to ↑ GFR
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how can NSAIDS cause kidney problems
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NSAIDs can cause acute renal failure in vascoconstrictive states by inhibiting the renal production of prostaglandins, which keep the afferent arterioles vasodilated to maintain GFR.
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causes of Respiratory acidosis
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–Acute lung disease –Chronic lung diseas –Opioids, narcotics, –Weakening of respiratory muscles –Airway obstruction
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causes of Metabolic acidosis with increased anion gap
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MUD PILES: Methanol Uremia Diabetic ketoacidosis Paraldehyde or Phenformin Iron tablets or INH Lactic acidosis Ethylene glycol Salicylates
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causes of Metabolic acidosis with normal anion gap
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–Hyperchloremia –Diarrhea –Glue sniffing –Renal tubular acidosis
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causes of Respiratory alkalosis
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–Hyperventilation –Aspirin ingestion (early)
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causes of metabolic alkalosis
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–Vomiting –Diuretic use –Antacid use –Hyperaldosteronism
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Anion gap = Na+ – (Cl – + HCO3 –)
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Na – (Cl + HCO3)
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Lab values for Respiratory acidosis
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pH < 7.4 PCO2 > 40 mmHg
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Lab Values For Metabolic acidosis with compensation
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pH < 7.4 PCO2 < 40 mmHg
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Lab Values For Respiratory alkalosis
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pH > 7.4 PCO2 < 40 mmHg
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Lab Values For Metabolic alkalosis with compensation
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pH > 7.4 PCO2 > 40 mmHg
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Potter’s syndrome cause
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Bilateral renal agenesis → oligohydramnios Caused by malformation of ureteric bud.
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Potter’s syndrome clinical findings
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limb deformities, facial deformities, pulmonary hypoplasia.
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Bilateral renal agenesis → oligohydramnios → limb deformities, facial deformities, pulmonary hypoplasia.
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Potter’s syndrome
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Horseshoe kidney describe
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Inferior poles of both kidneys fuse. As they ascend from pelvis during fetal development, horseshoe kidneys get trapped under inferior mesenteric artery and remain low in the abdomen.
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Horseshoe kidney who
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females with Turner Syndrome
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What casts in urine mean RBC casts
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glomerular inflammation (nephritic syndromes), ischemia, or malignant hypertension.
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What casts in urine mean WBC casts
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tubulointerstitial disease, acute pyelonephritis, glomerular disorders.
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What casts in urine mean Granular casts
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—acute tubular necrosis.
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What casts in urine mean Waxy casts
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—advanced renal disease/CRF.
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What casts in urine mean Hyaline casts
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—nonspecific.
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Presence of casts indicates that hematuria/pyuria is
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is of renal origin.
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What type of cast is seen in nephritic syndromes
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RBC casts
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What type of cast is seen in acute pyelonephritis
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WBC casts
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What type of cast is seen in acute tubular necrosis.
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Granular casts
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What type of cast is seen in advanced renal disease/CRF.
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Waxy casts—
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Characteristics of NephrItic syndrome
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I = inflammation. hematuria, hypertension, oliguria, azotemia.
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Characteristics of NephrOtic syndrome
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O = prOteinuria. massive proteinuria (frothy urine), hypoalbuminemia, peripheral and periorbital edema, hyperlipidemia.
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6 examples of NephrItic syndrome
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1. Acute poststreptococcal glomerulonephritis 2. Rapidly progressive (crescentic)glomerulonephritis 3. Goodpasture’s syndrome 4. Membranoproliferative glomerulonephritis 5. IgA nephropathy (Berger’s disease) 6. Alport’s syndrome
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6 examples of NephrOtic syndrome
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1. Membranous glomerulonephritis 2. Minimal change disease (lipoid nephrosis) 3. Focal segmental glomerular sclerosis. 4. Diabetic nephropathy 5. SLE 6. Amyloidosis
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LM/EM/IF findings in Acute poststreptococcal glomerulonephritis
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glomeruli enlarged and hypercellular, neutrophils, “lumpy-bumpy.”
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LM/EM/IF findings in Rapidly progressive glomerulonephritis
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—LM and IF: crescent-moon shape.
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LM/EM/IF findings in Goodpasture’s syndrome
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(type II hypersensitivity)—IF: linear pattern, anti-GBM antibodies.
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LM/EM/IF findings in Membranoproliferative glomerulonephritis
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—EM: subendothelial humps, “tram track.”
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LM/EM/IF findings in IgA nephropathy (Berger’s disease)
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—IF and EM: mesangial deposits of IgA.
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LM/EM/IF findings in Alport’s syndrome
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—split basement membrane.
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LM/EM/IF findings in Membranous glomerulonephritis
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LM: diffuse capillary and basement membrane thickening. IF: granular pattern. EM: “spike and dome.”
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LM/EM/IF findings in Minimal change disease
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LM: normal glomeruli. EM: foot process effacement
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LM/EM/IF findings in Focal segmental glomerular sclerosis
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LM: segmental sclerosis and hyalinosis.
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LM/EM/IF findings in Diabetic nephropathy
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LM: Kimmelstiel-Wilson “wire loop” lesions, basement membrane thickening (see Color Image 95).
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LM/EM/IF findings in 5. SLE
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(5 patterns of renal involvement) LM: In membranous glomerulonephritis pattern, wire-loop lesion with subepithelial deposits.
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LM/EM/IF findings in Amyloidosis
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IF: Congo red stain, apple green birefringence.
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Name the Glomerular pathology LM: crescent-moon shape.
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Rapidly progressive (crescentic) glomerulonephritis—
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Name the Glomerular pathology LM: glomeruli enlarged and hypercellular, neutrophils,
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Acute poststreptococcal glomerulonephritis
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Name the Glomerular pathology “lumpy-bumpy.”
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Acute poststreptococcal glomerulonephritis
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Name the Glomerular pathology EM:subepithelial humps. IF: granular pattern.
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Acute poststreptococcal glomerulonephritis
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Name the Glomerular pathology IF: crescent-moon shape.
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Rapidly progressive (crescentic) glomerulonephritis—
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Name the Glomerular pathology IF: linear pattern antibodies.
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Goodpasture’s syndrome (type II hypersensitivity)
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Name the Glomerular pathology EM: subendothelial humps, “tram track.”
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Membranoproliferative glomerulonephritis
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Name the Glomerular pathology “tram track.”
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Membranoproliferative glomerulonephritis
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Name the Glomerular pathology IF and EM: mesangial deposits of IgA.
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IgA nephropathy (Berger’s disease)
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Name the Glomerular pathology split basement membrane.
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Alport’s syndrome—
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Name the Glomerular pathology LM: diffuse capillary and basement membrane thickening.
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Membranous glomerulonephritis
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Name the Glomerular pathology IF: granular pattern. EM: “spike and dome.”
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Membranous glomerulonephritis
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Name the Glomerular pathology “spike and dome.”
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Membranous glomerulonephritis
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Name the Glomerular pathology EM: foot process effacement
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2. Minimal change disease (lipoid nephrosis)
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Name the Glomerular pathology LM: segmental sclerosis and hyalinosis.
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Focal segmental glomerular sclerosis
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Name the Glomerular pathology LM: Kimmelstiel-Wilson “wire loop” lesions, basement membrane thickening
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Diabetic nephropathy
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Name the Glomerular pathology (5 patterns of renal involvement)—LM: In membranous glomerulonephritis pattern, wire-loop lesion with subepithelial deposit
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SLE
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Name the Glomerular pathology IF: Congo red stain, apple green birefringence.
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Amyloidosis
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clinical features of Glomerular pathology Acute poststreptococcal glomerulonephritis
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Most frequently seen in children. Peripheral and periorbital edema. Resolves spontaneously.
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clinical features of Glomerular pathology Rapidly progressive (crescentic) glomerulonephritis
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Rapid course to renal failure. Number of crescents indicates prognosis.
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clinical features of Glomerular pathology Goodpasture’s syndrome
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(type II hypersensitivity) anti-GBM antibodies Hemoptysis, hematuria.
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clinical features of Glomerular pathology Membranoproliferative glomerulonephritis
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Slowly progresses to renal failure.
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clinical features of Glomerular pathology IgA nephropathy (Berger’s disease)
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Mild disease. Often postinfectious.
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Collagen IV mutation. Nerve deafness and ocular disorders.
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Alport’s syndrome
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clinical features of Glomerular pathology Alport’s syndrome
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Collagen IV mutation. Nerve deafness and ocular disorders.
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clinical features of Glomerular pathology Membranous glomerulonephritis
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Most common cause of adult nephrotic syndrome.
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Most common cause of adult nephrotic syndrome.
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Membranous glomerulonephritis
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clinical features of Glomerular pathology Minimal change disease
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Most common cause of childhood nephrotic syndrome. Responds well to steroids.
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clinical features of Glomerular pathology Focal segmental glomerular sclerosis
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More severe disease in HIV patients.
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clinical features of Glomerular pathology Diabetic nephropathy
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DM
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Most common cause of childhood nephrotic syndrome. Responds well to steroids.
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Minimal change disease (lipoid nephrosis)
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Glomerular pathology Amyloidosis associations
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Associated with multiple myeloma, chronic conditions,TB, rheumatic arthritis.
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Glomerular pathology Associated with multiple myeloma, chronic conditions,TB, rheumatic arthritis.
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Amyloidosis
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Minimal change disease aka
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lipoid nephrosis
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lipoid nephrosis aka
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Minimal change disease
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Kidney stones which are Radilucent.
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“I can’t C U on XRay.” for Cystine and Uric acid stones.
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Kidney stones which are Radopaque
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Calcium Ammonium magnesium phosphate (struvite)
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Most common kidney stones
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Calcium (75–85%): Calcium oxalate, calcium phosphate, or both.
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2nd most common kidney stone
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Ammonium magnesium phosphate (struvite)
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Conditions that cause hypercalcemia (??????) can lead to hypercalciuria and stones.
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cancer, ↑ PTH, ↑ vitamin D, milk-alkali syndrome
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Kidney stones that tend to recur
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Tend to recur.
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Kidney stones Radiopaque and Worsened by alkaluria.
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Ammonium magnesium phosphate (struvite)
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Kidney stones Radiolucent and Worsened by aciduria.
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Uric acid
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Kidney stones cause of Ammonium magnesium phosphate (struvite)
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Caused by infection with urease-positive bugs (Proteus vulgaris, ) Staphylococcus, Klebsiella).
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Kidney stones Can form staghorn calculi
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Ammonium magnesium phosphate (struvite)
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Kidney stones Uric acid associations
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Strong association with hyperuricemia (e.g., gout).
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Kidney stones Strong association with hyperuricemia (e.g., gout).
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Uric acid stone
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Kidney stones Uric acid who
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Often seen as a result of diseases with ↑ cell turnover, such as leukemia and myeloproliferative disorders.
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cause of Cystine Kidney stones
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Most often 2° to cystinuria.
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Most common renal malignancy
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Renal cell carcinoma
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Renal cell carcinoma who gets it and risk factors
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Most common in men ages 50–70. ↑ incidence with smoking and obesity.
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Renal cell carcinoma associations
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von Hippel–Lindau and gene deletion in chro- mosome 3.
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Renal cell carcinoma Histo
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Originates in renal tubule cells → polygonal clear cells.
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Renal cell carcinoma Clinical findings
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hematuria, palpable mass, 2° polycythemia, flank pain, fever, and weightloss.
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Renal cell carcinoma invasion features
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Invades IVC and spreads hematogenously.
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Renal cell carcinoma wrt paraneoplastic syn- dromes
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(ectopic EPO, ACTH, PTHrP, and prolactin)
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Most common renal malignancy of early childhood
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Wilms’ tumor
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Wilms’ tumor who
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Most common renal malignancy of early childhood (ages 2–4)
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Wilms’ tumor presentation
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Presents with huge, palpable flank mass, hemihypertrophy.
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Wilms’ tumor genetics
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Deletion of tumor suppression gene WT1 on chromosome 11.
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Wilms’ tumor WRT a complex
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WAGR complex: Wilms’ tumor, Aniridia, Genitourinary malformation, and mental-motor Retardation.
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WAGR complex
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WAGR complex: Wilms’ tumor, Aniridia, Genitourinary malformation, and mental-motor Retardation.
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Most common tumor of urinary tract system
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Transitional cell carcinoma
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Transitional cell carcinoma where
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(can occur in renal calyces, renal pelvis, ureters, and bladder).
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Painless hematuria
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is suggestive of bladder cancer
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Transitional cell carcinoma associations
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problems in your Pee SACS: Phenacetin, Smoking, Aniline dyes, Cyclophosphamide, Schistosomiasis
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Acute Pyelonephritis what is effected
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Affects cortex with relative sparing of glomeruli/vessels.
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pathognomonic for Acute Pyelonephritis
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White cell casts in urine
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Acute Pyelonephritis presentation
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Presents with fever, CVA tenderness.
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Chronic Pyelonephritis gross
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Coarse, asymmetric corticomedullary scarring, blunted calyx.
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Chronic Pyelonephritis casts
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eosinophilic
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thyroidization of kidney
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Chronic Pyelonephritis
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Acute generalized infarction of cortices of both kidneys
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Diffuse cortical necrosis
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what is Diffuse cortical necrosis
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Acute generalized infarction of cortices of both kidneys
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Diffuse cortical necrosis causes
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Likely due to a combination of vasospasm and DIC. Associated with obstetric catastrophes (e.g., abruptio placentae) and septic shock.
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what is Drug-induced interstitial nephritis
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Acute interstitial renal inflammation.
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Drug-induced interstitial nephritis presentation
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Fever, rash, eosinophilia, hematuria 2 weeks tis after administration.
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Drug-induced interstitial nephritis causes and mech
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Drugs (e.g., penicillin derivatives, NSAIDs, diuretics) act as haptens inducing hypersensitivity.
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Most common cause of acute renal failure.
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Acute tubular necrosis
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Acute tubular necrosis course
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Reversible, but fatal if left untreated. Recovery in 2–3 weeks.
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Acute tubular necrosis causes
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Associated with renal ischemia (e.g., shock), crush injury (myoglobulinuria), toxins.
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Acute tubular necrosis when do people die
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Death most often occurs during initial oliguric phase.
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Acute tubular necrosis mech
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Loss of cell polarity, epithelial cell detachment, necrosis, granular casts.
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Acute tubular necrosis stages
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Three stages: inciting event → maintenance (low urine) → recovery.
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Renal papillary necrosis associations
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1. Diabetes mellitus 2. Acute pyelonephritis 3. Chronic phenacetin use (acetaminophen is phenacetin derivative) 4. Sickle cell anemia
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what is Acute renal failure
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Abrupt decline in renal function with ↑ creatinine and ↑ BUN over a period of several days.
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Abrupt decline in renal function with ↑ creatinine and ↑ BUN over a period of several days.
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Acute renal failure
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Acute renal failure Prerenal azotemia Mech
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decreased RBF (e.g., hypotension) → ↓ GFR. Na /H2O retained by kidney.
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Acute renal failure Intrinsic mech
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generally due to acute tubular necrosis or ischemia/toxins. Patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule → ↓ GFR.
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Acute renal failure Intrinsic casts
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Urine has epithelial/granular casts.
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Acute renal failure Post renal mech
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3. Postrenal—outflow obstruction (stones, BPH, neoplasia). Develops only with bilateral obstruction.
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Consequences of renal failure
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0. Uremia 1. Anemia 2. Renal osteodystrophy 3. Hyperkalemia, 4. Metabolic acidosis 5. Uremic encephalopathy 6. Sodium and H2O excess 7. Chronic pyelonephritis 8. Hypertension
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mechanisms for the consequences of renal failure Uremia
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clinical syndrome marked by ↑ BUN and ↑ creatinine and associated symptoms.
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mechanisms for the consequences of renal failure Anemia
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(failure of erythropoietin production)
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mechanisms for the consequences of renal failure Renal osteodystrophy
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(failure of active vitamin D production)
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consequences of renal failure Hyperkalemia
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can lead to cardiac arrhythmias
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mechanisms for the consequences of renal failure Metabolic acidosis
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↓ acid secretion and ↓ generation of HCO3–
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consequences of renal failure Sodium and H2O excess →
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CHF and pulmonary edema
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2 forms of renal failure with causes
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acute renal failure (often due to hypoxia) and chronic renal failure (e.g., due to HTN and diabetes).
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what is Fanconi's syndrome
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Defect in proximal tubule transport of amino acids, glucose, phosphate, uric acid, protein, and electrolytes.
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Defect in proximal tubule transport of amino acids, glucose, phosphate, uric acid, protein, and electrolytes.
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what is Fanconi's syndrome
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Fanconi's syndrome complications
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rickets, osteomalacia, hypokalemia, metabolic acidosis.
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Adult polycystic kidney disease gross
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Multiple, large, bilateral cysts that ultimately destroy the parenchyma.
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Adult polycystic kidney disease presentation
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flank pain, hematuria, hypertension, urinary infection, progressive renal failure.
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Adult polycystic kidney disease Genes
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Autosomal dominant mutation in APKD1
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Adult polycystic kidney disease Associated with
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polycystic liver disease, berry aneurysms, mitral valve prolapse, diverticulosis
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Adult polycystic kidney disease cause of death
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from uremia or hypertension.
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Juvenile polycystic kidney disease gross
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radial cysts presentation in parenchyma
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Juvenile polycystic kidney disease genes
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Autosomal recessive.
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Juvenile polycystic kidney disease Associated with
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hepatic cysts and fibrosis.
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Dialysis cysts
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Cortical and medullary cysts resulting from long-standing dialysis.
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Simple cysts
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Benign, incidental finding. Cortex only.
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Medullary cystic disease describe and prognosis
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Medullary cysts. Ultrasound shows small kidney. Poor prognosis.
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Medullary sponge disease describe and prognosis
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Collecting duct cysts. Good prognosis.
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Na+ Low serum concentration vs High serum concentration
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Disorientation, stupor, coma Neurologic: irritability, delirium, coma
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Cl- Low serum concentration vs High serum concentration
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2° to metabolic alkalosis 2° to non–anion gap acidosis
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K+ Low serum concentration vs High serum concentration
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U waves on ECG, flattened T waves, arrhythmias, paralysis Peaked T waves, arrhythmias
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Ca2+ Low serum concentration vs High serum concentration
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Tetany, neuromuscular irritability Delirium, renal stones, abdominal pain
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Mg2+ Low serum concentration vs High serum concentration
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Neuromuscular irritability, arrhythmias Delirium, ↓ DTRs, cardiopulmonary arrest
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PO4 2− Low serum concentration vs High serum concentration
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Low-mineral ion product causes bone loss High-mineral ion product causes metastatic calcification, renal stones
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Name the Electrolyte disturbances Disorientation, stupor, coma
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Low Na+
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Name the Electrolyte disturbances 2° to metabolic alkalosis
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Low Cl−
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Name the Electrolyte disturbances U waves on ECG, flattened T waves, arrhythmias, paralysis
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Low K+
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Name the Electrolyte disturbances Tetany, neuromuscular irritability
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Low Ca2+
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Name the Electrolyte disturbances Neuromuscular irritability, arrhythmias
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Low Mg2+
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Name the Electrolyte disturbances Low-mineral ion product causes bone loss
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Low PO42−
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Name the Electrolyte disturbances Neurologic: irritability, delirium, coma
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High Na+
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Name the Electrolyte disturbances 2° to non–anion gap acidosis
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High Cl−
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Name the Electrolyte disturbances Peaked T waves, arrhythmias
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High K+
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Name the Electrolyte disturbances Delirium, renal stones, abdominal pain
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High Ca2+
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Name the Electrolyte disturbances Delirium, ↓ DTRs, cardiopulmonary arrest
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High Mg2+
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Name the Electrolyte disturbances High-mineral ion product causes metastatic calcification, renal stones
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High PO42−
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Mannitol Mechanism
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Osmotic diuretic, ↑ tubular fluid osmolarity, producing ↑ urine flow.
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Mannitol Clinical use
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Shock, drug overdose, ↓ intracranial/intraocular pressure
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Mannitol Toxicity
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Pulmonary edema, dehydration. Contraindicated in anuria, CHF.
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Acetazolamide Mechanism
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Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and reduction in total-body HCO3– stores.
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Acetazolamide Clinical use
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Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness.
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Acetazolamide Toxicity
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Hyperchloremic metabolic acidosis (ACIDazolamide causes ACIDosis), neuropathy, NH3 toxicity, sulfa allergy.
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Furosemide Mechanism
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Sulfonamide loop diuretic. Inhibits cotransport system (Na+, K+, 2 Cl −) of thick ascending limb of loop of Henle. Abolishes hypertonicity of medulla, preventing concentration of urine.
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Furosemide Clinical use
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Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia.
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Furosemide Toxicity
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OH DANG! Ototoxicity, Hypokalemia (↑ Ca2+ excretion. Loops Lose calcium.) Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout.
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Ethacrynic acid Mechanism
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Phenoxyacetic acid derivative (NOT a sulfonamide). Essentially same action as furosemide.
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Ethacrynic acid Clinical use
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Diuresis in patients allergic to sulfa drugs.
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Ethacrynic acid Toxicity
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Similar to furosemide; can be used in hyperuricemia, acute gout (never used to treat gout).
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Hydrochlorothiazide Mechanism
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Thiazide diuretic. Inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of the nephron. ↓ Ca2+ excretion.
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Hydrochlorothiazide Clinical use
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Hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus.
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Hydrochlorothiazide Toxicity
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Hypokalemic metabolic alkalosis, hyponatremia, Sulfa allergy. HyperGLUC: hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia.
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K+-sparing diuretics names
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EATS K+ Eplereone. Amiloride, Triamterene, Spironolactone,
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K+-sparing diuretics Mechanism
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Spironolactone is a competitive aldosterone receptor antagonist in the cortical collecting tubule. Triamterene and amiloride act at the same part of the tubule by blocking Na+ channels in the CCT.
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K+-sparing diuretics Clinical use
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Hyperaldosteronism, K+ depletion, CHF.
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K+-sparing diuretics Toxicity
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Hyperkalemia, endocrine effects (e.g., spironolactone causes gynecomastia, antiandrogen effects).
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Which diuretic causes gynecomastia, antiandrogen effects
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Spironolactone
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Diuretics: electrolyte changes Urine NaCl
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↑ (all diuretics—carbonic anhydrase inhibitors, loop diuretics, thiazides, K+-sparing diuretics).
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Diuretics: electrolyte changes Urine K+
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↑ (all except K+-sparing diuretics).
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Diuretics: electrolyte changes Blood pH
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↓ (acidosis)—carbonic anhydrase inhibitors, K+-sparing diuretics; ↑ (alkalosis)—loop diuretics, thiazides.
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Diuretics: electrolyte changes Urine Ca+
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↑ loop diuretics, ↓ thiazides.
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ACE inhibitors Mechanism
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Inhibit angiotensin -converting enzyme, reducing levels of angiotensin II and preventing inactivation of bradykinin, a potent vasodilator. Renin release is ↑ due to loss of feedback inhibition.
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ACE inhibitors Clinical use
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Hypertension, CHF, diabetic renal disease.
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ACE inhibitors Toxicity
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CHAPTOPRIL. Cough, hyperkalemia, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II.
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ACE inhibitors when to avoid them
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bilateral renal artery stenosis.
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Order of diuretic action as you go though the nephron
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1. Acetazolamide 2. Osmotic agents (mannitol) 3. Loop agents (e.g., furosemide) 4. Thiazides 5. Potassium sparing 6. ADH antagonists
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Name the diuretic by its toxicity Pulmonary edema, dehydration. Contraindicated in anuria, CHF.
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Mannitol
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Name the diuretic by its toxicity Hyperchloremic metabolic acidosis,
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Acetazolamide
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Name the diuretic by its toxicity ototoxicity
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Furosemide
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Name the diuretic by its toxicity Nephritis
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Furosemide
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Name the diuretic by its toxicity Hypokalemic metabolic alkalosis
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Hydrochlorothiazide
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Name the diuretic by its toxicity hyperGlycemia
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Hydrochlorothiazide
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Name the diuretic by its toxicity Hyperkalemia
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K+-sparing diuretics
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Name the diuretic by its toxicity endocrine effects
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spironolactone
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Name the diuretic by its toxicity gynecomastia
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spironolactone
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Name the diuretic by its toxicity antiandrogen
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spironolactone
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Name the diuretic used for Hyperaldosteronism
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K+-sparing diuretics
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Name the diuretic used for K+ depletion
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K+-sparing diuretics
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Name the diuretic used for Shock and drug overdose
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Mannitol
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Name the diuretic used for ↓ intracranial/intraocular pressure.
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Mannitol
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Name the diuretic used for Glaucoma,
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Acetazolamide
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Name the diuretic used for urinary alkalinization and metabolic alkalosis
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Acetazolamide
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Name the diuretic used for altitude sickness.
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Acetazolamide
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Name the diuretic used for Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema),
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Furosemide
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Name the diuretic used for hypertension and hypercalcemia.
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Furosemide or Hydrochlorothiazide
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Name the diuretic used for Diuresis in patients allergic to sulfa drugs.
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Ethacrynic acid
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Name the diuretic used for nephrogenic diabetes insipidus.
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Hydrochlorothiazide
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Types of renal tubular acidosis
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all (ecxept type 4) have high urine pH -Type 1: defect in H+ pump -Type 2: Renal loss of Bicarb -Type 3: genetic defect in type 2 carbonic anhydrase -Type 4: Hypoaldosteronism leading to hyperkalemia leading to inhibition of ammonia excretion
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what is renal tubular acidosis
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a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine
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a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine
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renal tubular acidosis
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