USMLE - Renal Part 2

Increased reabsorption of Na

| Increased secretion of K and H

DO Insulin LAB

| Digitalis, HyperOsmolarity, Insulin deficiency, Lysis of cells, Acidosis, Beta Antagonists

"Insulin shifts K into cells"

| Hypo-osmolarity, Insulin, Alkalosis, Beta agonists

Nausea, Malaise, Stupor, Coma

Irritability, stupor, coma

U wave, Flat T wave, Arrhythmias, muscle weakness

Wide QRS and peaked T waves, Arrhythmias, muscle weakness

Tetany, seizures

Stones (renal stones), Bones (pain), Groans (abdominal pain), Psychiatric overtones (anxiety, altered mental status), but not necessarily calcinuria

Tetany, arrhythmias

"Lazy DR. Better Hike/Cram Ca"

| Lethargy, decreased deep tendon reflexes, bradycardia, hypotension, cardiac arrest, hypocalcemia

Bone loss, osteomalacia

Renal stones, metastatic calcifications, hypocalcemia

Low pH, Low PCO2, Low [HCO3], Immediate hyperventilation

High pH, High PCO2, High [HCO3], Immediate hypoventilation

Low pH, High PCO2, High [HCO3], Delayed increase in bicarb reabsorption

High pH, Low PCO2, Low [HCO3], Decreased renal bicarb reabsorption

pH = 6.1 + log ([HCO3]/.(.03 x PCO2))

Winters Formula: PCO2 = (1.5 x [Bicarb]) + 8) +/- 2

| If not as predicted: Mixed acid/base disorder

Na - (Cl + HCO3)

| Normally 8-12 mEq/L

Hypoventilation due to Obstruction, Disease, Opioids or Sedatives, Muscle weakness

MUDPILES

Methanol (formic acid), Uremia, Diabetic ketoacidosis, Propylene glycol, Iron tablets or INH, Lactic acidosis, Ethylene glycol (Oxalic Acid), Salicylates (late)

HARD ASS

| Hyperalimentation, Addisons Disease, Renal Tubular Acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion

Hyperventilation (i.e. altitude sickness)

| Salicylates (early)

Loop Diuretics, Vomiting, Antaacids, Hyperaldosteronism

Defect in DT ability to excrete H
Urine pH > 5.5
Associated with HypoK
Increased risk for CaPO4 kidney stones because of increased urine pH and bone resorption

Defect in PT HCO3 reabsorption

Seen in Fanconi Syndrome

Urine pH < 5.5

Associated with hypoK

Increased risk for hypophosphatemic rickets

Low Aldosterone or lack of response to aldosterone --> hyperK --> impaired ammoniagenesis in PT --> PT loses buffering capacity --> urine pH decreases

Renal (vs. Bladder) origin

Glomerulonephritis, Ischemia, MalHTN

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

Oval Fat Bodies

| Indicate Nephrotic Syndrome

ATN

Advanced renal disease, Chronic renal failure

Non-specific. Can be a normal finding

Bladder Cancer or Kidney Stones

Acute Cystitis

<50% glomeruli involved

50% glomeruli involved

Hypercellular glomeruli

Thickening of glomerular BM

Only glomeruli involved

Glomeruli + other organ involved

"PARIS"
PSGN, RPGN, Berger's IgA Glomerulonephrtopathy, Alport Syndrome
(DPGN and MPGN can also be nephrotic)
(SLE can also cause a nephritic syndrome)
"PIG ARMS" includes Goodpastures and MPGN

"F. SAM M.D."
Focal Segmenting Glomerulosclerosis, Amyloidosis, SLE, Membranous Nephropathy, Minimal Change Disease, Diabetic Glomerulonephropathy
(DPGN and MPGN can also be nephritic)

"Protein LEACHs out"
Proteinuria > 3.5 g/day, ↑Lipids, Edema, hypoAlbuminia, ↑Cholesterol, HTN (Na retention)
Fatty Casts
Associated with Thromboembolism (hypercoagulable state due to ATIII loss)
Increased risk for infection (from loss of gamma Igs)

LM: segmental sclerosis and hyalinosis
EM: effacement of foot processes
Most common nephrotic syndrome in adults
Associated with HIV, Heroin, Obesity, Interferon treatment, Chronic kidney disease (due to congenital absence or removal)

"MP"

Subepithelial IC deposition

LM: Diffuse capillary and BM thickening

EM: "Spike and Dome" with subepithelial deposits

IF: Granular (IgG and C3)

SLE's presentation

2nd most common Nephrotic in adults

Causes: idiopathic, drugs, infections, SLE, tumors

T Cell Cytokines
LM: normal
EM: foot process effacement
Selective loss of albumin, not globins, because of BM polyanion loss
Triggered by recent infection or immune stimulus
Most common in children
Responds to corticosteroids

LM: congo red stain shows apple-green birefringence under polarized light
Associated with chronic conditions like Multiple Myeloma, TB, and RA

Subendothelial IC deposits
IF: Granular
Tram-Track appearance due to BM splitting caused by mesangial ingrowth
HBV, HCV

Intramembranous IC deposits
AutoAb --/ degradation of C3 convertase which leads to low levels of C3
"Dense deposits"
Associated with C3 nephritic factor

Nonenzymatic Glycosylation of BM --> ↑ permeability to proteins + ↑ thickness
NEG of EA --> hyaline arteriolosclerosis --> ↑GFR --> hyperfiltration --> damage to mesangial cells --> mesagnial expansion
Osmotic damage to glomerular capillary endothelial cells (Glucose --> sorbitol which is osmotically active and leads to swelling and cellular damage)

ATIIR --> IP3

| ATIIR --/ cAMP

Cytokines damage podocytes causing them to fuse and destroy - charge of GBM

Both. 1 (40%) > 2 (20%)

LM: Mesangial expansion, BM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson Lesion)

Inflammatory Process mediated by neutrophils

"PR HOZ"

Proteinuria (<3.5g/day)

RBC casts

Hematuria, HTN (due to salt retention)

Oliguria

aZotemia

"Throat, Bloat, Coke"
Child w/ previous infection (GAS), peripheral + periorbital edema, HTN, and dark urine
Resolves Spontaneously

LM: Glomeruli enlarged and hypercellular. Neutrophils, "lumpy bumpy"
EM: Subepithelial IC humps
IF: Granular appearance due to IgG, IgM and C3 deposition along BM and mesangium

LM + IF: crescent moon shape

| Crescents = fibrin + plasma proteins (C3) with glomerular parietal cells, monocytes, and macs

Poor (days to weeks)

Goodpasture's (hematuria + hemoptysis), Wegener's (cANCA), Microscopic polyangiitis (pANCA)

Type II Hypersensitivity Rxn

| Abs to GBM + alveolar BM

Linear pattern

Subendothelial IC mediated

SLE + MPGN cause it

LM: wire looping of capillaries

EM: subendothelial and sometimes intramembranous IgG-based IC often with C3 deposition

IF: granular

DPGN

SLE and MPGN

"AM" Think Mesangium

Related to Henoch-Schonlein Purpura

LM: mesangial proliferation

EM: mesangial IC deposits

IF: IgA based IC deposits in mesangium

Often presents/flares with URI or acute gastroenteritis

Small vessels

Most common vasculitis in children

"NAPA"

Child following URI with Nephropathy, Abdominal pain (melena), Purpura, Arthralgia

Mediated by IgA complex deposition

Associated with IgA nephropathy

Multiple lesions of same age

Small vessels

Upper Respiratory Tract: Perforated nasal septum, sinusitis, otitis media, mastoiditis

Lower RT: Hemoptysis, Cough, Dyspnea

Renal: Hematuria, RBC Casts

Focal Necrotizing vasculitis + Necrotizing granulomas in the lung and upper airway + Necrotizing glomerulonephritis

c-ANCA

Large Nodular Densities

Cyclophosphamide and corticosteroids

"Imagine the V in IV splitting the BM"
Mutation in IV collagen --> split basement membrane
X linked
Glomerulonephritis, deafness, eye problems

Fluid intake

80%
CaPO4 --> ↑pH
CaOxalate --> ↓pH
Radiopaque

Ethylene glycol or VitC abuse

Thiazide and citrate

CaOxalate stone in pt with hypercalcinuria and normocalcemia

15%
Precipitates at ↑pH
Radiopaque

Caused by infection with urease+ bugs (proteus mirabilis, Staph, Klebsiella)
The bugs hydrolyze urea to ammonia and this alkalizes urine
Can form staghorn calculi that can be a nidus for UTIs

5%
Precipitates at ↓pH
RadiolUcent

Visible on CT and US but not XR
Associated with hyperuricemia (gout)
Often seen in diseases with high cellular turnover (leukemia)
Treat w/ alkalinization of urine

Cystine Kidney Stones

Frequency

Precipitates at pH

XR

Usually Secondary to

Appearance of stone

Treatment

Backup of urine into the kidney
Caused by urinary tract obstruction or vesicoureteral reflux
Leads to dilation of renal pelvis and calyces
Results in parenchymal thinning

Most common cause of intrinsic renal failure
Self reversible in some cases but can be fatal if untreated
Death most often occurs during oliguric phase

Renal ischemia (from shock, sepsis)

Crush injury (myogloniburia)

Drugs, toxins

Initiation: Ischemic injury. Usually unnoticed

Maintenance

Recovery:

Oliguria. Low Urine Osm.

Fluid overload (edema)

Increased Cr/BUN,

Increased K. High Na excretion.

Anion Gap Met Acidosis (because of retention of H and anions).

Muddy Brown Casts.

Last 1-3 days

Diuresis, Hypotonic urine, Low K, Mg, PO4, and Ca

Sloughing of renal papillae
Gross hematuria and proteinuria
May be triggered by a recent infection or immune stimulus
Associated with DM, Acute Pyelonephritis, Chronic Phenacetin Use (acetaminophen)
Sickle Cell Anemia

Abrupt decline in renal function with ↑ Cr and ↑ BUN over several days

↓RBF --> ↓GFR

| BUN/Cr ↑

Generally due to ATN or ischemia/toxins
Less commonly due to acute glomerulonephritis
Necrosis --> debris obstructing tubule --> fluid back flow --> ↓GFR
Epithelial/granular casts
BUN/Cr ↓

Due to outflow obstruction (stones, BPH, neoplasia, congenital abnormalities)
Develops only with bilateral obstruction

Urine Osm (mOsm/kg) > 500
Urine Na (mEq/L) < 20 FENa < 1% BUN/Cr > 20

Urine Osm (mOsm/kg) < 350 Urine Na (mEq/L) > 40
FENa > 2%
BUN/Cr < 15

Urine Osm (mOsm/kg) < 350 Urine Na (mEq/L) > 40
FENa > 2%
BUN/Cr > 15

Na/Water retention --> CHF, Pul Edema, HTN)

HyperK

Met Acidosis

Uremia

Anemia (low EPO)

Renal Osteodystrophy

Dyslipidemia (↑ Tris)

Growth retardation and developmental delay (children)

↑BUN and ↑Cr

| Nausea, anorexia, Pericarditis, Asterixis, Encephalopathy, Platelet dysfunction

Low VitD + Kidney dysfunction --> ↓Ca and ↑PO4 --> ↑PTH --> bone resorption (subperiosteal thinning of bone)

Multiple, large, bilateral cysts
Flank pain, hematuria, HTN, Urinary infections, Progressive renal failure
Autosomal Dominant in PKD1 or 2 on chromosome 16
Death from chronic kidney disease or HTN (↑ Renin)
Associated with Berry Aneurysm, MVP, Benign Hepatic cysts

Autosomal recessive
Associated with hepatic fibrosis
In utero --> Potters
Beyond neonatal concerns --> HTN, Portal HTN, Progressive renal insufficiency

Autosomal dominant

Leads to tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine

Medullary cysts usually not visualized

US: shrunken kidney

Poor prognosis

Originates from PT cells

Polygonal clear cells (accumulated lipids and Carbs)

Most common in Men 50-70

Risk ↑ w/ smoking and obesity

Hematuria, palpable mass, polycythemia, flank pain, fever, wt loss

Renal vein --> IVC

Lung and Bone

Most common renal cancer
Gene deletion in chromosome 3 (sporadic or von Hippel Lindau)
Paraneoplastic (EPO, ACTH, PTH)
Silent cancer because retroperitoneal. Usually detected b/c of metastases
Resection. Resistant to Chemo and Radiation

Most common renal malignancy of early childhood (2-4)
Contains embryonic glomerular structures
Presents with huge palpable flank mass and/or hematuria
Deletion of tumor suppressor WT1 on chromosome 11
May be part of Beckwith-Wiedemann Syndrome

WARG

| Wilms, Aniridia, Genitourinary malformations, Retardation

Most common tumor of urinary tract system
Can occur in Calyces, pelvis, ureters, bladder
Painless hematuria (no casts)
"problems in the Pee SAC"
Phenacetin, Smoking, Aniline dyes, Cyclophosphamide

Affects cortex with sparing of glomeruli and vessels
Fever, CVA tenderness, nausea, vomiting
White cell casts in urine

Result of recurrent episodes of acute pyelonephritis
Requires predisposition to infection (vesicoureteral reflux, chronic kidney stones)
Coarse, asymmetric corticomedullary scarring and blunted calyx
Tubules can contain eosinophilic casts (thyroidization of kidney)

Azotemia, fever, rash, hematuria, CVAT. Can be asymptomatic
Pyuria (eosinophils)
Drugs act as haptens --> hypersensitivity
1-2 weeks: Diuretics, penicillin, sulfonamide, rifampin
Months: NSAIDs

Acute generalized cortical infarction of both kidneys
Combination of vasospasms and DIC
Associated with obstetric catastrophe (abruptio placentae) and Septic Shock

PSGN

| Membranous

MPGN I

| DPGN

Charges in the Tubule of the Kidney

PT: -4
LoH: +7
DT: -10
CT: -50