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65 Cards in this Set

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Minimal Change Disease
LM- Normal Glom
EM- Foot process effacement
Lab- Selective loss of albumin, Not Igs due to GBM polyanion loss
Cause- Possibly due to recent infection or immune stimulus. Most common in children. Also associated with nodular sclerosing Hodgkin's lymphoma. Responds to steroids.
Focal Segmental Glomerulosclerosis
LM- Segmental sclerosis and hyalinosis
Cause- Associated with HIV
Membranous GN
LM- Diffuse thickening of the capillary wall and GBM
EM- SUBEPITHELIAL Ig-containing deposits along the GBM that are separated by small, spikelike protrustions of GBM (Spike and Dome)
IF- Granular deposits
Cause- Infections (HBV), drugs (penicillamine, captopril, NSAIDs), solid tumors (lung, colon, melanoma), SLE. MCC of adult nephrotic syndrome.
Membranoproliferative GN- Type I
Cause- HBV, HCV, SLE. Caused by circulating ICs
LM- Glom are large with an accentuated lobular appearance, thick GBM, capillary wall shows double contour (Tram tracking) due to GBM splitting from mesangial ingrowth.
Membranoproliferative GN- Type II
Cause- C3 nephritic factor (an auto-antibody against C3 convertase that stabilizes the enzyme to cause uncontrolled activation of the alternate pathway.
EM- Dense deposits
LM- Congo red stain, apple-green bifirengence; Thick GBM and mesangium. Nephrotic syndrome
Diabetic glomerulonephropathy
NEG of GBM leads to permeability and thickening. NEG of efferent arterioles leads to increased GFR and mesangial expansion.
LM- mesangial expansion, GBM thickening, nodular glomerulosclerosis (Kimmelstiel-Wilson lesion)
Cause- Most frequently seen in children (skin infection first). Present with peripheral and periorbital edema, increased ASO titers, anti DNAse B, decreased complement, and hypertension. Cola colored urine (gross hematuria)!
LM- Glom are enlarged and hypercellular, neutrophils, "lumpy-bumpy" appearance
IF-granular with IgG, IgM, C3 deposits in the GBM and mesangium (starry sky)
RPGN (crescentic)
For all: LM and IF have a crescent moon shape, consisting of fibrin and plasma proteins with glomerular function parietal cells, monocytes, and macrophages.
1. Goodpasture syndrome- Type II, Abs to GBM and alveolar BM (alpha3 of type IV collagen). Linear deposits of IgG and c3 on GBM. Patients have hematuria and hemoptysis.
2. Wegener's granulomatosis- cANCA; nasomucosal ulcers
3. Microscopic polyangitis- pANCA
Diffuse proliferative GN (due to SLE or MPGN)
LM- Wire looping of capillaries
IFs- granular
IgA nephropathy (Berger's disease)
Cause- Presents with URI or acute gastroenteritis (synpharyngitic nephritis) 2-3 days later. Occurs in children with painless hematuria.
LM/IF- IC (IgA) deposits in mesangium.
Alport's syndrome
Cause- Mutation in type IV collagen (a5 chain abnormality of type IV collagen leads to lack of a3 chain- predisposed to Goodpasture's). Nerve disorders, ocular disorders, X-linked dominant
LM- Split basement membrane; foam cells in glomerulus
Acute pyelonephritis (TIN)
Organisms- E. coli (most common), Proteus, Klebsiella, Enterobacter, Pseudomonas.
Clinical- Patients present with CVA tenderness, fever, N/V. Associated with urinary obstruction, instrumentation, vesicoureteral reflux, pregnancy, DM. Leukocyte esterase (+). WBC casts in urine!
Pathology- Glomeruli spared. Neutrophils in tubules and abscess formation. Affects the cortex
Chronic pyelonephritis (TIN)
Course, asymmetric corticomedullary scarring, blunted calyx. Diffuse interstitial fibrosis. Tubules contain eosinophilic casts (thyroidization of kidney)
Drug-induced interstitial nephritis
Causes- Penicillins (methicillin, ampicillin), rifampin, sulfonamides, NSAIDs, thiazides. These act as haptens and induce hypersensitivity.
Clinical- Pyuria (eosinophils) and azotemia 1-2 weeks after administration of drugs. A/w fever, rash, hematuria, and CVA tenderness
Renal Papillary necrosis
Causes- DM, acute pyelonephritis, chronic phenacetin and acetaminophen use (analgesic nephropathy), sickle cell anemia!!!!!!
Pathology- Ischemic and suppurative necrosis at the tips of the renal pyramids (papillae). The papillae slough off, causing gross hematuria and proteinuria. Coagulative necrosis is present.
Acute Tubular necrosis
MCC of acute renal failure in the hospital. Reversible if treated. 3 stages: inciting event, maintenance (low urine output), and recovery (early on there is a steady increase in urine volume up to 3L, electrolyte imbalances- death, 2-3 weeks by tubular re-epithelialization). See granular brown casts in urine!
Associated with- renal ischemia (shock, sepsis), crush injury (myoglobinuria), toxins (aminoglycosides + IV contrast). TAL and PCT MOST SUSCEPTIBLE!
What is clearance?
C = Urine [X] x Urine flow rate / plasma [X]
What factors affect GFR?
GFR = Kf [(Pgc - Pbc) - oncontic gc)]
What does PAH clearance approximate?
EFFECTIVE renal plasma flow (EPRF underestimates RPF by about 10%)
How does constriction of a ureter affect GFR and RPF?
RPF doesn't change
GFR decreases
When does glucosuria begin? When are all the transporters saturated?
160-200 mg/dL glucosuria begins; all transporters are saturated by 350 mg/dL
Where in the nephron does PTH act?
At the PCT it blocks the Na/phosophate cotransport to facilitate phosphate excretion. At the DCT it activates the Ca/Na exchanger to reabsorb calcium
What are the actions of AII?
1. Acts at vascular smooth muscle to vasoconstrict and increase bp.
2. Constricts efferent arteriole to increase GFR and FF. Unlike ANP, there IS a compensatory increase in Na reabsorption.
3. Regulates aldosterone secretion from the adrenal gland.
4. Increases ADH release from the posterior pituitary
5. Increases proximal Na/H activity (permits contraction alkalosis) for H2O reabsorption.
6. Stimulates thirst in the hypothalamus.
What are the actions of aldosterone?
1. Increases ENac, Na/K ATPase insertion in the principle cells of the CCD.
2. Enhances K and H excretion
What does ANP do?
Relaxes smooth muscles via cGMP to increase GFR and decrease renin (decreases bp and promotes diuresis). Na filtration is increased, but there is no corresponding compesatory increase in reabsorption so there is Na and volume loss.
What secretes renin?
JG cells (modified smooth muscle cells of the afferent arteriole) in response to decreased renal blood pressure, decreased sodium delivery to the distal tubule (sensed by macula densa), and increased sympathetic tone (B1)
What shifts K out of cell (cause hyperkalemia)?
Insulin deficiency
Acidosis, severe exercise
Cell lysis
What shifts K into cells? (hypokalemia)
What metabolic disturbance is seen in salicylate toxicity?
Metabolic acidosis, respiratory alkalosis, normal pH
What is Winter's formula?
P(CO2) = 1.5 (HCO3) + 8 +/-2
What are causes of metabolic alkalosis?
Diuretic use (chloride decreases, contraction alkalosis)
Vomiting (Cl low)
Antacid use
Hyperaldosteronism *urine chloride increases*
What are causes of AG metabolic acidosis?
MUDPILES- Methanol, uremia, DKA, paraldehyde/phenformin, Iron tablets or INH, Lactic acidosis, Ethylene glycol, Salicylates
What are causes of normal AG metablic acidosis?
Diarrhea, glue sniffing, RTA, hyperchloremia
What is type 1 RTA?
Defect in collecting tubules ability to excrete H+. Associated with hypokalemia and risk of calcium-containing kidney stones.
What is type 2 RTA?
Defect in proximal tubule HCO3 reabsorption. Associated with hypokalemia and hypophosphatemic rickets.
What is type 4 RTA?
Hypoaldosteronism or lack of response to aldosterone. Associated with hyperkalemia and inhibition of ammonium excretion in the proximal tubule. Urine pH is decreased due to decreased buffering capacity. MCC is DM (destroy JGA).
What is associated with RBC casts?
Acute glomerulonephritis, ischemia, or malignant hypertension
What is associated with WBC casts?
Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
What is associated with granular (muddy brown) casts?
What is associated with fatty casts with maltese crosses?
Nephrotic syndrome
What causes calcium stones?
Calcium oxalate (MC), calcium phosphate, or both. Conditions that cause hypercalcemia (cancer, increased PTH, excess vitamin D, milk alkali syndrome, sarcoidosis), oxalate crystals from ethylene glycol or vitamin C abuse, Crohns disease
What makes ammonium magnesium phosphate (struvite) stones worse?
What type of stone is radiolucent?
Uric acid- see in diseases with high cell turnover; worse with acidic pH of urine
How do you diagnose cystine stones?
Cyanide-Nitroprusside test: CN converts cystine to cystein, which can bind nitroprusside and change the urine to purple
How do you treat cystine stones?
Alkalinize the urine
Where does RCC originate?
Proximal tubular cells
How does RCC metastasize?
Hematogenously- Renal vein to IVC
What is the triad associated with RCC?
Painless hematuria, palpable abdominal mass, dull flank pain
What paraneoplastic syndromes are associated with RCC?
EPO, ACTH, PTHrP, prolactin
What is the WAGR complex?
Wilms tumor, Aniridia (no iris), GU malformation, and mental Retardation
What conditions is transitional cell carcinoma associated with?
Phenacetin, Smoking, Analine dyes, Cyclophosphamide

Associated with painless hematuria (bladder)
Diffuse cortical necrosis
Acute generalized cortical infarction of one or both kidneys due to a combination of vasospasm and DIC. Associated with obstetric complications and septic shock.
What is seen in pre-renal azotemia?
-Increased BUN/Cr: GFR decreases with Na/H2O and urea retained by the kidney to conserve volume.
-This can be caused by dehydration, hypovolemia, shock, renal VC (NSAIDs)
-Decreased urine osmolarity
What is seen in renal azotemia?
-Usually due to ATN or ischemia/toxins (not really due to GN). GFR is decreased due to patchy necrosis and debris obstructing the tubule. Urine will have epithelial/granular casts
-BUN reabsorption is impaired because of the kidney disease so BUN/Cr decreases
What is seen in post-renal azotemia?
-Due to outflow obstruction (stones, BPH, neoplasia, congenital). Only happens if the obstruction is bilateral.
-FeNa is increased (>4%), BUN/Cr is normal initially but may decrease if no relief of obstruction.
What are the consequences of renal failure?
-Na/H2O retention leads to CHF, Pulmonary edema, and HTN.
-Hyperkalemia leads to arrhythmias
-Metabolic acidosis
-Uremia (clinical- nausea, anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction)
-Anemia (failure of EPO)
-Renal osteodystrophy (can lead to secondary PTH)
-Dyslipidemia (increased TGs)
-Growth retardation and developmental delay in kids
What conditions are ADPKD associated with?
MVP, berry aneurysms, polycystic liver disease
What is ARPKD associated with?
Congenital hepatic fibrosis, portal hypertension, progressive renal insufficiency
What is medullary cystic disease?
Also called sponge kidney; Can lead to fibrosis and progressive renal insufficiency with urinary concentrating defects; US will show a small kidney
What part of the kidney does ADH act upon?
The MEDULLARY collecting duct!!!! Principle cells
What is the reabsorption rate?
Reabsorption = Filtered - Excreted = (GFR x Px) - (V x Ux)
What is secretion rate?
Secretion = Excretion - Filtered =
(V x Ux) - (GFR x Px)
What is the filtered load?
GFR x plasma concentration
What bacteria are associated with ammonium magnesium phosphate (struvite) stones?
Urease positive- Staph, Proteus, Klebsiella