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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