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