Renal Flashcards
most common site of obstruction
Ureteropelvic junction
Potter sequence (syndrome) sx
Oligohydramnios → compression of developing fetus → limb deformities, facial anomalies (low-set ears, retrognathia, flattened nose), compression of chest and lack of amniotic fluid aspiration into fetal lungs pulmonary hypoplasia (cause of death)
Causes of Potter sequence
ARPKD, obstructive uropathy, bilateral renal agenesis, chronic placental insufficiency
On what vessel does a horseshoe kidney get trapped?
Under IMA and remain low in the abdomen
What do you have increased risk of in duplex collecting system?
UTIs
Course of ureters
Pass under uterine artery or under vas deferens (retroperitoneal)
Best estimate of GFR
Creatinine clearance
Best estimate of RPF
PAH clearance
Equation for filtration fraction
FF = GFR/RPF
Normal FF?
20%
Where is glucose reabsorbed?
In the proximal convoluted tubule (PCT) by Na+/glucose cotransport
Plasma glucose threshold for glucosuria? When are all transports saturated?
∼ 200 mg/dL
∼ 375 mg/min
What is absorbed in the early PCT?
all glucose and amino acids and most HCO3, Na, Cl, PO43, K, H2O, and uric acid
Effect of PTH at the PCT?
inhibits Na/PO43 cotransport → PO43 excretion
Effect of ATII at the PCT?
Stimulates Na/H exchange → ↑ Na, H2O, and HCO reabsorption (permitting contraction alkalosis)
Tonicity of filtrate leaving the PCT?
Isotonic
What occurs in the thin descending loop of Henle?
Passive reabsorbtion of H2O via medullary hypertonicity (impermeable to Na+) Concentrating segment. Makes urine hypertonic
Which section of the kidney is the “concentrating segment”
thin descending loop of Henle
What occurs in the thick ascending loop of Henle?
Reabsorbs Na, K, and Cl
Indirectly induces paracellular reabsorption of Mg2+ and Ca2+ through ⊕ lumen potential
What happens to the concentration of urine in the TAL?
Makes urine less concentrated as it ascends; impermeable to H2O
What happens to the concentration of urine in the DCT?
Makes urine fully dilute (hypotonic)
PTH effect on DCT?
↑ Ca2/Na exchange: Ca2+ reabsorption
Aldosterone regulation in the collecting tubule?
reabsorbs Na+ in exchange for secreting K+ and H+
ADH effect in collecting tubule?
acts at V2 receptor to ↑ aquaporins on apical side
Order of Na reabsorption
Early PCT > TAL > DCT > CD
Fanconi syndrome
Generalized reabsorptive defect in PCT
↑ excretion of all amino acids, glucose, HCO3, and PO4; leads to metabolic acidosis
Causes of Fanconi Syndrome
hereditary defects (eg, Wilson disease, tyrosinemia, glycogen storage disease, cystinosis), ischemia, multiple myeloma, nephrotoxins/drug, lead poisoning (Fanconi is First dx in renal tubule)
Bartter syndrome
AR reabsorptive defect in thick ascending loop of Henle
Affects Na/K/2Cl cotransporter → hypokalemia and metabolic alkalosis with hypercalciuria
Presents like loop diuretic use
Gitelman syndrome
AR reabsorptive defect of NaCl in DCT
HypoK, hypoMg, metabolic alkalosis, hypocalciuria
Presents like thiazide use
Liddle syndrome
GoF: ↑ Na+ reabsorption in collecting tubules d/t ↑ Na channel activity
HTN, hyperK, metabolic alkalosis, ↓ aldosterone
Looks like hyperaldosteronism except aldosterone is zero
Treat w/ amiloride
Syndrome of Apparent Mineralocorticoid Excess
Hereditary deficiency of 11β-hydroxysteroid dehydrogenase: converts cortisol to cortisone in cells with MC-r
↑ MC activity: HTN, hypoK, metabolic alkalosis
Can happen w/ too much licorice
Treat with corticosteroids
Distal renal tubular acidosis
Type 1; pH > 5.5
Defect in ability of α intercalated cells to secrete H → no new HCO3 → metabolic acidosis
Hypokalemia, Ca phosphate stones
Causes of Type 1 RTA
Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract
Proximal renal tubular acidosis
Type 2
Defect in PCT HCO reab
Hypokalemia, hypophosphatemic stones
Causes of type 2 RTA
Fanconi syndrome and carbonic anhydrase inhibitors
Hyperkalemic renal tubular acidosis
Type 4
D/t Hypoaldosteronism
Hyperkalemia
Casts in urine
Indicates glomerular or renal tubular
ie. not bladder cancer or infection or kidney stones
RBC casts
Glomerulonephritis, malignant hypertension
WBC casts
Tubulointerstitial in ammation, acute pyelonephritis, transplant rejection
Fatty casts (“oval fat bodies”)
Nephrotic syndrome. Associated with “Maltese cross” sign
Granular (“muddy brown”) casts
Acute tubular necrosis
Waxy casts
End-stage renal disease/chronic renal failure
Hyaline casts
Nonspecific, can be a normal finding, often seen in concentrated urine samples
PSGN on LM, IF and EM
LM: glomeruli enlarged and hypercellular
IF: starry sky; granular
EM: subepithelial immune complex humps
RPGN on LM and IF
Crescent moon shape; crescents consist of brin and plasma proteins with glomerular parietal cells, monocytes, macrophages
Diffuse proliferative glomerulonephritis on LM, EM and IF
LM—“wire looping” of capillaries EM—subendothelial and sometimes intramembranous IgG-based ICs with C3 deposition IF—granular
Dz associated with diffuse proliferative glomerulonephritis
SLE
IgA nephropathy on LM, EM and IF
LM: mesangial proliferation
EM: mesangial IC deposits
IF: IgA-based IC deposits in mesangium
Alport syndrome
Type IV collagen; Xlinked
“Basket-weave” on EM
Lens dislocations, glomerulonephritis, sensorineural deafness
Membrano- proliferative glomerulonephritis
Type I: subendothelial immune complex with granular IF; “tram-track”; GBM splitting
Type II: DDD
Cause of type I Membrano- proliferative glomerulonephritis
2° to hepatitis B or C infection or idiopathic
Cause of type II Membrano- proliferative glomerulonephritis
C3 nephritic factor (IgG antibody that stabilizes C3 convertase)
FSGS on LM, IM and EM
LM: segmental sclerosis and hyalinosis
IF: ⊝, but may be ⊕ for nonspecific focal
deposits of IgM, C3, C1
EM: effacement of foot process like MCD
Most common cause of nephrotic syndrome in African Americans and Hispanics
FSGS
Membranous nephropathy on LM, IF, and EM
LM: diffuse capillary and GBM thickening
IF: granular d/t immune complex deposition; nephrotic presentation of SLE
EM: “spike and dome” appearance with subepithelial deposits.
Most common cause of 1° nephrotic syndrome in Caucasian adults
Membranous nephropathy
Diabetic glomerulo- nephropathy on LM
Mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis
Most common cause of end-stage renal disease in the United States
Diabetic glomerulo- nephropathy
Ammonium magnesium phosphate stone
↑ pH; Radiopaque
Coffin lid shaped
Urease ⊕ bugs
Form staghorn calculi
Uric acid stone
↓ pH; Radiolucent
Rhomboid or rosettes
Gout and ↑ cell turnover (leukemia)
Cystine stone
↓ pH; Radiolucent
Hexagonal
Hereditary: lost function of cystine reabsorbing PCT transporter
Sodium cyanide nitroprusside test ⊕
Calcium stone
Most common; Radiopaqu
oxalate > phosphate
↓ pH
Hydronephrosis
Distention/dilation of renal pelvis and calyces
Renal cell carcinoma
From PCT cells: polygonal clear cells filled with lipids and carbohydrates (golden-yellow)
Most common 1° renal malignancy
RCC spread
Invades renal vein (may develop varicocele if left sided) then IVC and spreads hematogenously; metastasizes to lung and bone
Renal oncocytoma
Benign epithelial cell tumor from collecting ducts
Large eosinophilic cells with abundant mitochondria without perinuclear clearing
Nephroblastoma
Wilms tumor
Contains embryonic glomerular structures
LoF of WT1 or WT2 on 11
WAGR complex
Denys-Drash
Wilms tumor, early-onset nephrotic syndrome, male pseudohermaphroditism (WT1 mutation)
Beckwith-Wiedemann
Wilms tumor, macroglossia, organomegaly, hemihyperplasia (WT2 mutation)
Transitional cell carcinoma
Painless hematuria (no casts) Most common tumor of urinary tract system
Squamous cell carcinoma of the bladder
Squamous metaplasia → dysplasia and squamous cell carcinoma
Risk: Schistosoma infection (Middle East), chronic cystitis, smoking, cx nephrolithiasis
Painless hematuria
Stress incontinence
Urethral hypermobility or intrinsic sphincteric defciency
Leak w/ ↑ intra-abdominal pressure
⊕ bladder stress test
Urgency incontinence
Overactive bladder (detrusor instability): leak with urge to void immediately
Over flow incontinence
Incomplete emptying (detrusor underactivity or outlet obstruction): leak with overfilling
Acute pyelonephritis histology
Neutrophils in ltrate renal interstitium; WBCs in urine +/− WBC casts
Affects cortex with relative sparing of glomeruli/vessels
Acute pyelonephritis presentation
Fevers, flank pain, nausea/vomiting, chills
Chronic pyelonephritis appearance
Coarse, asymmetric corticomedullary scarring, blunted calyx
Tubules can contain eosinophilic casts resembling thyroid tissue
Chronic pyelonephritis risks
Predisposition to infection such as vesicoureteral reflux or chronically obstructing kidney stones
Xanthogranulomatous pyelonephritis
Rare; grossly orange nodules; mimic tumor nodules; widespread kidney damage due to granulomatous tissue containing foamy macrophages
Diffuse cortical necrosis
Acute generalized cortical infarction of both kidneys
D/t vasospasm or DIC
Strong association w/ obs problems
Acute tubular necrosis
Seen in hospitalized patients
Granular (“muddy brown”) casts
Spontaneously resolves
Renal papillary necrosis
Sloughing of necrotic renal papillae; gross hematuria and proteinuria
