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Flashcards in Renal Deck (76):

Pronephros, mesonephros, and metanephros

Pronephros: Present at week 4; later degenerates

Mesonephros: interim kidney for first trimester; later contributes to male genital system

Metanephros: appears in 5th wk gestation, forms permanent kidney. ureteric bud form mesonephric duct gives rise to ureter, pelvises, calyces, collecting ducts. metanephric mesenchyme gives rise to glomerulus through distal convoluted tubule


Potter sequence

Oligohydramnios causes compression of developing fetus leading to limb deformities and facial anomalies, compression of chest, lack of aspiration of fluid into fetal lungs leading to pulmonary hypoplasia

Causes: ARPKD, obstructive uropathy, bilateral renal agenesis


Horseshoe kidney

Inferior poles of kidneys fuse; gets trapped under inf mesenteric artery as kidneys ascend


Multicystic dysplastic kidney

Caused by abnormal interaction between ureteric bud and metanephric mesenchyme. Nonfunctional kidney of cysts and connective tissue


Duplex collecting system

bifurcation of ureteric bud creating bifid ureter; associated iwth vesicoureteral feflux, ureteral obstruction, UTIs


Path of ureters

Under uterine artery and under ductus deferens (water under the bridge)


Fluid breadkwon of body

60% of body made of water
40% ICF; 20% ECF


Glomerular giltration barrier

Filters plasma by size and charge. Consists of fenestrated endothelium, fused BM containing heparan sulfate (neg charge barrer), epithelial layer with podocyte foot processes


Formula for renal clearance

C=UV/P=volume of plasma from which substance completely cleared per unit time

U=urine concentration of X
P=plasma concentration of X
V=urine flow rate


Formula for GFR

GRF = clearance of inulin = Uinulin x V/Pinulin
works because inulin neither reabsorbed nor secreted


Filtration fraction

fraction of circulating plasma that gets filtered into the tubules

normal is 20%


Hartnup disease

AR deficiency of neutral amino acid transporters in proximal renal tubular cells and on enterocytes resulting in neutral aminoa cids in urine and decreased absorption from the gut

Results in pellagra like symptoms due to decreased tryptophan converstion to niacin


Function of early PCT

-reabsorbs all glucose and amino acids
-reabsorbs most ions isotonically
-generates and secretes NH3 to buffer secreted H+
-responds to PTH to decreased phosphate reabsorption
-responds to AT II to increase Na+ reabsortipon via Na+/H+ exchange (permits contraction alkalosis)


Function of loop of henle

Thin descending loop:
-passively reabsorbs H2O via medullary hypertonicity
-concentrates urine

Thick ascending loop
-reabsorbs Na+, K+, Cl-
-paracellular reabsorption of Mg++ and Ca++
-impermeable to water - makes urine less concentrated


Function of early DCT

-reabsorbs Na+ and Cl- making urine dilute
-increases Ca++ reabsorption in response to PTH


Function of collecting tubule

-reabsorbs Na+ in exchange for secretion of K+ and H+ (aldo regulated)
-reabsorbs more water in response to ADH


Aldosterone actions

All in collecting tubule
-principles cells: increases apical K+ conductance, increases Na+/K+ pump, increases ENaC channels
-intercalated cells: increases H+ ATPase activity which increases the HCO3-/Cl- exchanger


Fanconi syndrome

Reabsorptive defect in PCT. Increased excretion of amino acids, glucose, bicarb, and phosphate. Can cause metabolic acidosis.

Can be caused by ischemia, multiple myeloma, nephrotoxic drugs, lead poisoning


Bartter syndrome

Reabsorptive defect in thick ascending loop due to effect in Na+/K+/2Cl- co transporter. AR. Hypokalemia and metabolic alkalosis, hypercalciuria.


Gitelman syndrome

Reabsorptive defect of NaCl in DCT. AR. Hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria.


Liddle syndrome

AD gain of funtion mtation that increases Na+ reabsorption in collecting tubules


Syndrome of apparent mineralocorticoid excess

Deficiency of 11beta hydroxysteroid dehydrogenase: excess cortisol increases mineralocorticoid receptor activity leading to HTN, hypokalemia, metabolic alkalosis. Can acquire from licorice which blocks this enzyme.


Actions of angiotensin II (five)

-constricts efferent arteriole to increase filtration fraction and GFR despite low volume
-promotes aldosterone and ADH secretion
-increases Na+/H+ exchange in proximal collecting tubule
-stimulates hypothalamus leading to thirst


Stimuli for angiotensin II release (3)

Decreased BP sensed by JG cells
Decreased distal delivery of Na+ to macula densa cells
Increased sympathetic tone via beta1 receptors

All stimulate renin which leads to activation of angiotensinogen to angiotensin I


Activity of ANP and BNP

Released from atria and ventricles in response to increased volume. Relax vascular smooth muscle to increase GFR and decrease renin (check on RAAS system)


JG apparatus

Consists of mesangial cells, JG cells (modifed afferent arteriole smooth muscle), macula densa (NaCl sensor that is part of DCT)

Secretes renin in response to decreased renal BP and increased sympathetic tone


Prostaglandins in the kidney

Vasodilate afferent arteriole to increase RBF. Block by NSAIDs leads to constriction of afferent and decreased GFR


Things that shift K+ out of cells (six)

Do LABS: digitalis, hyperosmolarity, lysis of cells, acidosis, beta blocker, high blood sugar


things that shift K+ into cells (four)

Beta agonists


Presentation of hypo and hyperkalemia

Hypo: U waves, flattened waves, arrhythmia, muscle spasm

Hyper: Wide QRS, peaked T waves, arrhythmias, muscle weakness


Presentation of hypo and hypercalcemia

Hypo: tetany, seiqures, QT prolongation

Hyper: "stones, bones groans, thrones, and psychiatric overtones"
-renal stones
-bone pain
-abdominal pain
-increased urinary frequency
-anxiety and altered mental status


Presentation of hypo and hypermagnesemia

Hypo: tetany, torsades, hypokalemia

Hyper: decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia


Winters formula

Predicts respiratory comp for metabolic acidosis

PCO2=1.5[HCO2-] + 8 +/- 2


Renal tubular acidosis presentation

Normal anion gap metabolic acidosis with hypokalemia or hyperkalemia


Causes of RBC casts

glomerulonephritis, malignant HTN


Causes of fatty (oval body) casts

Nephrotic syndrome


causes of granular casts

ATN - muddy brown


causes of waxy casts

end stage renal disease/chronic renal failure


Pathology of post strep GN

Cause of nephritic syndrome. Granular immune complex and complement deposition in subepithelial space


Pathology of RPGN

crescent moon shape deposits

Goodpasture: linear antibody staining


Pathology and cause of diffuse proliferative glomerulonephritis

Causes: SLE, membranoproliferative GN

wire looping, subendothelial granular deposits

Presents with nephritic syndrome


IgA nephropathy

Episodic hematuria with RBC casts. Nephritic syndrome.

Mesangial pfolieration and immune complex deposits in mesangium


Alport syndrome

Causes nephritic syndrome, eye problems, deafness

x-linked mutation in type IV collagen

thinning and splitting of GBM with basket weave appearance on EM


membranoproliferative glomerulonephritis

Causes nephritic and nephrotic syndrome.

Type I: subendothelial complex deposits, tram track appearance due to GBM splitting, may be associated with hep B or C infection

Type II: intramembranous complex deposits, associated with C3 nephritic factor


Two complications of nephrotic syndrome

Hypercoagulable state due to antithrombin III loss in ruine
Increased risk of infection due to loss of Ig in urine


Focal segmental GN

Causes nephrotic syndrome (most common cause in blacks and hispanics)

Segmental scerlosis and halinosis. Focal deposits of IgM and C3. Foot process effacement

Inconsistent response to steroids; may progress to chronic renal disease


Minimal change disease

Causes nephrotic syndrome (most common cause in children). Can be triggered by recent infection or immunization.

Normal LM and IF with foot process effacement on EM

Excellent response to steroids


Membranous nephropathy

Most common cause of nephrotic syndrome in caucasian adults. Nephrotic presentation of SLE

Diffuse capillary and GBM thikening with granular immune complex deposition and spike and dome subepithelial deposits on EM

Poor response to steroids, may progress to chronic disease


Amyloidosis of kidney

Causes nephrotic syndrome (kidney most commonly involved organ)

Apple gree birefringence with congo red stain


Diabetic glomerulonephropathy

Causes nephrotic syndrome

Mesangial expansion and GBM thickening, eosinophilic nodular glomerulosclerosis, glycosylation of GBM


Presentation of kidney stones

Unilateral flank pain, colicky pain radiating to groin, hematuria


Calcium kidney stones

Radiopaque on X-ray. Envelope or dumbbell shaped stones. Calcium phosphate precipitates at increased pH, calcium oxalate at decreased pH.

Can occur with ethylene glycol, vit C abuse, hypocitraturia, malabsorption.

Treated with thiazides, hydration, citrate


Ammonium magnesium phosphate kidney stones

Radiopaque on X-ray. Precipitate at increased pH. Coffin lid urine crystals. Caused by infection with urease pos bugs that hydrolyze urea to ammonia, alkalinizing the urine. Can form staghorn calculi.

Treated by treating the infection and removing the stone surgically


Uric acid crystals

Radiolucent rhomboid or rosettes. Precipitate at decreased pH. Associated with hyperuricemia and increased cell turnover (leukemia)

Treat by alkalinizing the urine and with allopurinol


Cystine kidney stones

Radiolucent hexagonal stones. Precipitate at low pH. Hereditary: associated with loss of function of cystine reabsorption.

Seen in kids, can form staghorn calculi

Treated with alkalanization of urine

Diagnosed with sodium cyanide nitroprusside test


Renal cell carcinoma

Population: Men 50-70, higher risk with smoking and obesity, VHL syndrome

Presentation: Hematuria, palpable mass, secondary polycythemia, flank pain, fever. Can cause paraneoplastic syndrome. Often doesn't present until metastatic. Spreads by blood to lung and bone when invades renal vein.

Pathogenesis: Originates from PCT cells

Chemo and radiation resistant


Renal oncocytoma

Benign epithelial cell tumor. Well circumscribed. Large eosinophilic cells. Presents with painless hematuria, flank pain, abdominal mass


Wilms tumor

Also called nephroblastoma. Most common renal cancer in kids 2-4. Contains embryonic glomerular structures.

Presentation: large, palpable, unilateral flank mass and/or hematuria

Cause: loss of function mutations in WT1 or WT2. Can be part of Beckwith-Wiedemann syndrome or WAGR complex


Beckwith-Wiedemann syndrome

Wilms tumor


WAGR complex

Wilms tumor
GU malformation
Mental retardation


Transitional cell carcinoma

Occurs in urinary tract system: renal calyces, renal pelvis, ureters, bladder

Presents with painless hematuria

Risks: phenacetin, smoking, aniline dyes, cyclophosphamide


Squamous cell carcinoma of bladder

Chronic irritation of bladder leads to squamous metaplasia which leads to dysplasia and SCC

Risk factors: Schistosomal haematobium, chronic cystitis, smoking, chronic nephrolithiasis

Presentation: painless hematuria


Chronic pyelonephritis

Recurrent episodes of acute pyelo leads to scarring and blunted calyces with tubules containing eosinophilic casts resembling thyroid tissue

Associated with VU reflux or chronic kidney stones


Drug-induced interstitial nephritis

Pyuria (esp eosinophils) and azotemia 1-2 weeks after certain drugs - diuretics, penicillins, PPIs, sulfonamides, rifampin. Can occur months after starting NSAIDS

May be associated with fever, rash, hematuria, CVA tenderness


Diffuse cortical necrosis

Cortical infart of both kidneys

Presents with abrupt onset anuria, gross hematuria, flank pain

Associated with obstetric catastrphoes, septic shock


Acute tubular necrosis

Most common cause of AKI. Usually resolves spontaneously but can be fatal. Increased FENa.

Granular casts

Causes: ischemia, nephrotoxicity due to drugs, crush injury, hemoglobinuria


Renal papillary necrosis

Sloughing of necrotic renal papillae leading to gross hematuria and proteinuria.

Associated with sickle cell disease, acute pyelonephritis, NSAIDs, diabetes


Consequences of renal failure

-metabolic acidosis
-uremia: pericarditis and aterixis, encephalopathy, platelet dysfunction, N/V
-Na+ and water retention
-growth retardation/developmental delay
-EPO failure
-renal osteodystrophy



Mutation: PKD1 on chromosome 16 or PKD2 on chromosome 4, AD

Presentation: flank pain, hematuria, HTN, urinary infection, progressive renal failure in young adulthood. Bilateraly enlarged cystic kidneys

Associations: berry aneurysm, mitral valve prolapse, benign hepatic cysts



Mutation: AR mutation

Presentation: Systemic HTN, progressive renal insufficiency, portal HTN and congenital hepatic fibrosis in neonate. Can cause Potter sequence in utero


Medullary cystic disease

Inherited disease. Tubulointerstitial fibrosis and progressive renal insufficiency. Shrunken kidneys on US


ADH and urea

ADH increases water permeability of collecting ducts. Water leaves tubules causing urea concentration within the tubules to increase.

ADH activates urea transporters in medullary collecting duct so that mroe urea is reabsorbed and its clearance is decreased.

This increases urea in the medullary interstitium, increasing medullary osmotic gradient for water reabsorption


Acyclovir renal toxicity

Occurs in 5-10% of those receiving acyclovir IV. Concentration in collecting d;ct exceeds solubility resulting in crystallization and renal tubular damage. Prevented with hdyration


Tuberous sclerosis

AD condition

Cortical tubers and subependymal hamartomas in brain leading to seizures and mental retardation.

Also can see cardiac rhabdomyomas, facial angiofibromas, ash-leaf patches on skin, and renal angiomyolipomas.


Thrombocytopenic thrombotic purpora-hemolytic uremic syndrome

Pentad of fever, neurologic symptoms, renal failure, anemia, thrombocytopenia in setting of GI illness. Causes microvascular thrombosis in brain kidneys and heart and platelet activation in arterioles and capillaries


Myeloma cast nephropathy

Develops due to excess excretion of free light chains (bence Jones proteins). Proteins form casts that cause tubular obstruction and epithelial injury leading to impaired renal function. Biopsy shows glassy casts that stain eosinophilic