Path 20: Kidney no make pee Flashcards by Albert Bouwer

Post strep glomerulonephiritis timeline and IF/EM

1-4 weeks

Granular staining pattern for IgG and C3 humps of immune complexes

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Renal tubular acidosis types

1: Distal renal
2: Proximal renal
4: Hyperkalemic

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Distal renal tubular acidosis pathogenesis

Inability of α-intercalated cells to secrete H+

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Distal renal tubular acidosis findings

Decreased serum K+.

Urine pH above 5.5

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Renal tubular acidosi: what type of acidosis ?

Normal anion gap

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Proximal renal tubular acidosis pathogenesis

PCT HCO3 reabsorption is impaired leading to increased urine HCO3

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Hyperkalemic tubular acidosis pathogenesis

Hypoaldosterone or aldosterone resistance leads to hyperK. Leads to decreased NH4 excretion

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Labs in type 4 tubular acidosis

Increased serum K+

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Fanconi sx sumptoms

Generalized PCT reabsoroption defect. Leads to excretion of all PCT absorbed sunstances

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Barter syndrome pathogenesis and findings

Na/+K+/2Cl- defect

Acts like lasix

Metabolic alkalosis, hypoK, hypercalciuria

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Liddle syndrome caused by

Gain of function leads to decrease in Na+ degredation and increase in Na+ reabsorption in collecting tubule

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RBC casts seen with

Glomerolonephritis, HTN

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WBC casts seen in

Tubulointerstitial inflamation, pyelonephritis

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Granular casts seen in ? and appearance

Acute tubular necrosis

“Muddy brown”

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Fatty casts seen in and visual

Nephrotic syndrome

Maltese cross

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Waxy casts seen in

ESRF

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Neprhitic syndrome presentation

Hematuria, RBC casts, oligouria, HTN

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Nephritic syndrome etiology

Glomerula inflammation leads to GBM damage

Leads to RBC loss and hematuria

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Nephrotic syndrome etiology

Podocyte damage fucks with charge barrier leading to proteinuria

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Nephrotic syndrome findings

Massive proteinuria with edema, frothy urine, hypercoagulable state

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PSGN post strep pathology

2-4 weeks after strep infection. Type III hypersensitivity

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PSGN light IF

Starry sky/ granular appearance.

IgG, IgM and C3 deposition in GBM and mesangium

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PSGN Electron microscopy

Subepithelilial IC humps

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RPGN features

Rapid deterioration, cresents

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RPGN and linear IF:

Goodpasture syndrome (Type II hypersensitivity)

RPGN and negative IF:

Granulomatosis C-ANCA, MPO-ANCA, p-ANCA

RPGN and Granular IF

diffuse proliferative glomerulonephritis

Diffuse proliferative glomerulonephitis seen with

Lupus

Diffuse proliferative glomerulonephritis EM

Sub endothelial deposit

IgA nepropathy aka

Berger dx

Berger disease presentation

IGA vasculitis due to current GI/Resp infection

IgA nepropathy IF

On mesangium, granular

Alport syndrome pathogenesis

Type IV collagen mutation Glomerular basement membrane loss of integrity

Minimal change disease pathology

Nephrotic syndrome in children Due to foot process effacement

Focal segemental glomerulosclerosis LM/EM findings

LM: segemental sclerosis and hyalinosis EM: effacement of foot processes

Membranous nepropathy pathogenesis

Usually idiopathic GBM thickening

Membranous nepropathy LM/IF/EM findings

IF: granular LM: thick GBM and capillary EM: spike and dome subepithelial

Amylodisosis finding

Apple green birefringence

Diabetic glomerulonephropathy pathology

Hyperglycemia leads to glycation of proteins leads to increads GBM membrane. Causes hypterfiltration

Drugs that help diabetic nephropathy

ACE inhibitor

Calcium stone features

Radiopaque , can be calciuria,

Ammonium magnesium phosphate stones aka ____ + features

Struvite Radiopaque Caused by infections that hydrolyze urea Coffin cristal

Elevated urine ph causes precipitation of

Calcium phosphate Ammonium magnesium phosphate

Hypocitriuria causes precipitation of

Calcium oxalate

Decreased urine ph causes precipitation of

Uric acid Cystine

Uric acid stone features

Radiolucent Rhomboid crystal Seen in diseases with rapid cell turnover

Cystine stone features

Seen in cystinuria, hexagonal crystals

Staghorn caliculi stone types

Infections (struvite) Cystine

Chronic pyelonephritis pathology

Interstitial fifrosis, usually due to obstruction. Atrophic tubules lead to *thyrodization*

Prerenal azotemia due to

Hypovolemia

Prerenal azotemia BUN/CR

More than 20

Postrenal azotemia BUN:Cr

less than 15

Acute interstitial nephritis pathology

Drug induced hypersensitivity to NSAIDs, PCN and diuretics

Acute interstitial nephritis presentation

Oliguria, fever, rash. No pain. Pyuria, azotemia

Acute tubular necrosis presentation

Acute renal failure, hyperK, metabolic acidosis, uremia, increased FENA+, unconcentrated urine

Renal papillary necrosis presentation

Gross hematuria and flank pain, often inciting event

Renal failure consequences

Metabolic acidosis HyperK Sodium retention

Autosomal dominant kidney disease presentation and gene Cysts where

APKD1/2 gene mutation. Presents as young adult with HTN and renal failure Cyts in medulla and cortex

autosomal dominant PKD treatment

ACE inhibitors ARBs

Autosomal recessive PKD features

Potter seuqnece, congenital hepatic fibrosis, cysts in collecting ducts .

Renal cell carcinoma presentation

Hematuria, papable mass, flank pain Fever, weight loss, paraneoplastic syndrome

Renal cell carcinoma gene progression

Loss of VHL gene (chromosome 3)

Most common malignant renal tumor in kids

Wilms tumor (avg 3yo)

Wilms tumor pahtology

Malignant tumor made of blastema (mesenchyme)

Wilms tumor presentation

Palapable mass, hematuria, HTN

Wilms tumor with no iris and malformed genitals

WAGR complex

wilms tumor with WT1 deletion

WAGR

Wilms tumor with hypoglycemia, hypertrophy of tongue and muscles (+gene)

Beckwith-Wiedman *WT2*

Membranous nepropathy caused by (virus)

HepB