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83 Cards in this Set
- Front
- Back
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RBC Casts
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1. glomerulonephritis
2. ischemia 3. malignant HTN |
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WBC Casts
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1. tubulointerstitial inflammation
2. acute pyelo 3. transplant rejection |
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Granular "muddy brown" casts
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acute tubular necrosis
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Waxy casts
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advanced renal disease/CRF
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Hyaline casts
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nonspecific
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No casts
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bladder cancer (hematuria)
kidney stones (hematuria) acute cystitis (pyuria) |
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Type 1 RTA
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Distal
Impaired H+ excretion in collecting tubule Hypokalemia and risk for Ca kidney stones |
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Type 2 RTA
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Proximal
Impaired bicarb reabsorption in proximal tubule Hypokalemia and hypophosphatemic rickets |
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Type 4 RTA
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Collecting tubule
Due to hypoaldosteronism or lack of collecting tubule response to aldo Hyperkalemia Inhbition of ammonium excretion in proximal tubule --> decreased urine pH due to decreased buffering capacity |
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Type IV collagen mutation
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Alport's
Nephritic syndrome Collagen defect causes split basement membrane also have ocular disorders, nerve disorders, deafness (x-linked) |
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ICs in mesangium
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Berger's disease
aka IgA golmerulopathy nephritic syndrome often presents with a URI or acute gastroenteritis |
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Wire looping of capillaries on LM
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"Wire Loopus"
DPGN (which is due to SLE or MPGN) Nephritic syndrome MCC death in SLE |
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Subendothelial DNA-anti-DNA ICs
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DPGN (which is due to SLE or MPGN)
Nephritic syndrome MCC death in SLE |
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Anti-GBM antibodies causes type II hypersensitivity
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Goodpasture's
example of RPGN (crescentic) Nephritic syndrome IF: linear |
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crescent-moon shape of fibrin and plasma proteins with parietal cells, monocytes, macrophages
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Rapidly progressive GN (crecentic)
poor prognosis, rapidly deteriorating renal function Ex: Goodpasture's: type II hypersenstivity; anti-IgG to GBM and alveolar BM; linear IF -anti-collagen IValpha3 chain Wegener's: c-ANCA Microscopic polyangiitis: p-ANCA |
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Subepithelial IC humps
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Acute post-strep GN
also see "lumpy-bumpy glomeruli with hypercellular neutrophils IF: granular starry sky ASO titers, anti-DNAse B, decreased C3, anti-cationic proteinase children; peripheral and periorbital edema resolves spontaneously |
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Amyloidosis
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Nephrotic syndrome
congo red stain, apple-green birefringence associated with MM, TB, RA |
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Spike and dome appearance with subepithelial deposits
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Membranous glomerulonephritis (diffuse membranous glomerulopathy)
see diffuse capillary and GBM thickening on LM Can be caused by drugs, infections, SLE, solid tumors |
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Minimal Change Disease
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LM: nl glomeruli
EM: foot process effacement selective loss of albumin, no globulins *children may be triggered by infxn or immune stimulus Tx: corticosteroids |
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mesangial expansion, GBM thickening, nodular glomerulosclerosis
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= Kimmelstiel-Wilson lesion in
Diabetic glomerulonephropathy NephrOtic syndrome Due to nonenzymatic glycosylation of GBM and efferent arterioles (which increases GFR) |
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Segmental sclerosis and hyalinosis
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Focal segmental glomerulosclerosis
MC adult NephrOtic syndrome (and MC in HIV patients) |
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tram-track appearance on LM
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Type I Membranoproliferative GN
NephrOtic syndrome, but can also present as nephritic syndrome Associated with HBV, HCV subendothelial ICs with granular IF tram-track due to GBM splitting caused by mesangial ingrowth |
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subendothelial ICs
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1. MPGN
2. SLE 3. DPGN (nephritic syndrome that can be caused by MPGN or SLE) |
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NephrOtic syndrome
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massive prOteinuria (>3.5g/day), frothy urine, hyperlipidemia, fatty casts, edema
assoc with thromboembolism and increase risk of infxn (loss of Igs) FAD MMM FSGS Amyloidosis Diabetic Membranous Membranoproliferative Minimal change disease (lipoid nephrosis) |
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Nephritic syndrome
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Inflammatory
hematuria and RBC casts azotemia, oliguria, HTN, proteinuria (<3.5g/day) AABCD 1. Acute post-strep 2. Alport's 3. Berger's disease (IgA glomerulopathy) 4. Crescentic: Rapidly progressive glomerulonephritis 5. Diffuse porliferative glomerulonephritis (due to SLE or MPGN) |
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SLE nephropathy
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nephrotic syndrome: membranous glomerulonephritis
nephritic syndrome: DPGN (MCC death in SLE) |
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dense deposits on EM
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Type II Membranoproliferative GN
NephrOtic syndrome (can also present as nephritic) Associated with C3 and nephritic factor |
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IF: granular IC deposition
LM: diffuse capillary thickening |
membranous GN
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IF: granular pattern of IC deposition
LM: hypercellular glomeruli |
post-strep GN
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IF: linear IC deposition
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RPGN (Goodpasture's)
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IF: deposition of IgG, IgM, IgA, and C3 in mesangium
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IgA nephropathy
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Glomerular filtration barrier
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according to size and net charge
1. Fenestrated capillary endothelium: size 2. Fused b.m. with heparan sulfate: negative charge barrier 3. Epithelial layer with podocyte foot processes *charge barrier lost in nephrotic syndrome |
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Renel Clearance
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Cx = Ux*V / Px
Cx<GFR: net reabsorption Cx>GFR: net secretion Cx=GFR: no net secretion or reabsorption (i.e. inulin, creatinine) |
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GFR & ERPF
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Normal GFR ~ 100ml/min
Creatinine clearance slightly overestimates GFR bc Cr is moderately secreted by renal tubules Effective renal plasma flow ERPF: estimated using PAH clearance bc both filtered and actively secreted *all PAH entering kidneys is excreted ERPF underestimates true RPF by ~10% |
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Changes in glomerular dynamics
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Afferent arteriole constriction:
decrease RPF, decrease GFR Efferent arteriole constriction: decrease RPF, increase GFR Increase plasma protein: only decrease GFR Decrease plasma protein: only increase GFR Constriction of ureter: only decrease GFR |
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Glucose clearance
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at normal plasma level: completely reabsorbed in prox tubule by Na/glu cotransport
160-200: glucosuria begins 350: all transporters fully saturated (Tm) |
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Early proximal tubule
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reabsorbs ALL glucose and AA
most bicarb, NaCl, H2O Isotonic absorption generates and secretes ammonia, which acts as a buffer for secreted H+ PTH: inhibits Na/Phosphate cotransport (excretion) ATII: stimulates Na/H exchange --> increase Na and H2O reabsorption (get contraction alkalosis) |
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Thin descending loop of Henle
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Passive reabsorption of H20 via medullary hypertonicity (impermeable to Na).
Concentrating segment. Makes urine hypertonic |
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Thick ascending loop of henle
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reabsorbs Na, K, Cl
reabsorbs Mg and Ca (paracellularly) Impermeable to H20 Dilutes urine |
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Early DCT
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active reabsorption of NaCl
Diluting segment Makes urine hypotonic PTH: increases Ca/Na exchange for Ca reabsorption |
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Collecting tubules
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Reabsorption of Na in exchange for secreting K and H+ (regulated by aldosterone)
Aldo: insert Na channel on lumen side ADH: insertion of aquaporin H2O channels on lumen side alpha intercalated cell: secrete acid, absorb K and bicarb beta intercalated cell: secrete bicarb, absorb Cl- and H+ |
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RAAS
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Cause renin secretion:
1. decrease BP (JG cells) 2. decrease Na (MD cells) 3. increase sympathetic tone (beta1) |
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Ang. II
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1. ATII receptors on vasc smooth muscle --> vasoconstriction
2. Constricts efferent arteriole of glomerulus --> increase GFR & FF 3. Aldosterone secretion from adrenals (Na reabsorption, K and H+ excretion) 4. ADH: H2O reabsorption 5. Increase prox tubule Na/H activity --> H2O reabsorption 6. Stimulates thirst centers in hypothalamus |
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Aldosterone
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primarily regulates blood volume
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ADH
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primarily regulates osmolarity, but also responds to low blood volume, which takes precedence
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ANP
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released from atria in response to increased vol.; relaxes vasc smooth muscle via cGMP --> increase GFR, decrease renin
causes increased GFR and Na filtration |
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JGA
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JG cells: modified smoothmuscle of afferent arteriole
Macula densa: Na+ sensor on DCT |
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Kidney endocrine functions
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1. EPO: released from endothelial cells of peritubular capillaries in response to hypoxia
2. Vit D: proximal tubule activates vit D with 1alpha-hydroxylase; activation stimulated by PTH 3. Renin 4. Prostaglandins: paracrine secretion vasodilates the afferent arterioles to increase GFR (NSAIDS can cause ARF) PTH: phosphate excretion in PCT; Ca reabsorption in DCT |
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Mg
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HypoMg: neuromusc irritability, arrhythmia
HyperMg: decreased DTRs, cardiopulmonary arrest |
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K
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HypoK:
U waves, flattened Ts, arrhythmias, paralysis HyperK: Peaked Ts, wide QRS, arrhythmias |
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AG metabolic acidosis
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AMUDPILES:
aspirin methanol (formic acid) uremia DKA paraldehyde, phenformin Iron, INH Lactic acidosis Ethylene glycol (oxalic acid) Sepsis, shock |
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normal AG metabolic acidosis
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8-12
diarrhea glue sniffing RTA hyperchloremia |
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Metabolic alkalosis
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Vomiting
diuretic use (contraction) antacid use hyperaldosteronism |
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Calcium oxalate stones
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can result from ethylene glycol
vitamin C abuse steatorrhea (calcium that normally binds oxalate forms a sopa with fat) |
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Struvite stones
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Amm Mg Phos
infxn with urease+: Proteus Staph Klebsiella can form staghorn calculi that can be a nidus for UTIs *worsened by alkaluria |
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Uric acid stone
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RadiolUcent
seen in disease with increased cell turnover (leukemia) |
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Cystine stone
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most often 2/2 cystinuria
*hexagonal crystals Cystinuria: AA transport defect; COLA (cystine, ornithine, lysine, arginine) in PCT tx: acetazolamide alkalinize urine |
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Renal Cell Carcinoma
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originates in renal tubular cells --> POLYGONAL CLEAR CELLS
RFs: smoking, obesity assoc with paraneoplastic syndromes: EPO, ACTH, PTHrP, PRL assoc with von Hippel-Lindau syndrome |
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Wilms' tumor
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nephroblastoma
MC renal malignancy of early childhood (2-4yo) contains embryonic glomerular structures *deletion of tumor suppressor gene WT1 on chr 11 |
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WAGR complex
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Wilms' tumor
Aniridia GU malformation Retardation: motor and mental |
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Hypocomplementemia
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Post-strep GN
MPGN (II) Lupus nephritis |
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Transitional cell carcinoma
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MC tumor of urinary tract system
*renal calyces, renal pelvis, ureters, bladder assoc with problems in your PeeSAC: Phenacetin Smoking Aniline dyes Cyclophosphamide |
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Chronic pyelo
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Asymmetric corticomedullary scarring, blunted calyx
*tubules can contain eosinophilic casts *thyroidization of kidneys (from expanded tubules) |
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Acute interstitial nephritis
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Pyuria (eos), azotemia
-occurs 1-2wks after taking a drug: diuretics, NSAIDs, PCN, sulfonamides, rifampin *drug acts as haptens, inducing hypersensitivity sxs: fever, rash, hematuria, CVA tenderness tx: 2 weeks of steroids |
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Diffuse cortical necrosis
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acute generalized cortical infarction of both kidneys
*likely do to a combo of vasospasm and DIC *obstetric catastrophes, septic shock |
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Acute tubular necrosis
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MCC ARF in hospital
*self-reversible, but fatal if left untreated 3 stages: 1. inciting event 2. maintenance: oliguria 3. recovery: 2-3wks cuases: ischemia, crush injury, toxins, drugs (AG, ceph, polymyxins), contrast, rhabdo *granular muddy brown casts |
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Renal papillary necrosis
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sloughing of renal papillae --> gross hematuria, proteinuria
may be triggered by a recent infection or immune stimulus PAP DAPS DM Acetaminophen (phenacetin) Pyelo SCA |
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Uremia
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consequence of renal failure
*increased BUN/Cr (azotemia) + sxs: nausea, anorexia pericarditis asterixis encephalopathy PLT dysfunction |
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ADPKD
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multiple large bilateral cysts that destroy parenchyma
hematuria, flank pain, HTN, UTI polycystic liver disease berry aneurysms MVP |
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ARPKD
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infants
auto recessive congenital hepatic fibrosis significant renal failure in utero --> Potter's (bilat renal agenesis) fetal u/s: enlarged kidneys, oligo hydramnios, absent or small bladder HTN, portal HTN, renal failure |
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Other cysts
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dialysis: cortical and medullary
simple: benign, common; thin fluid filled, nonenhancing, cortical medullary cystic disease: can lead to fibrosis and progressive renal failure; see small kidneys on U/S |
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Mannitol
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osmotic diuretic
increase tubular fluid osmolarity use: shock, drug OD, increased ICP (or intraocular pressure) tox: pulm edema, hyperNa, dehydration CI: CHF, anuria |
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Acetazolamide
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carbonic anhydrase inhibitor
NaHCO3 diuresis and reduction in total body bicarb use: glaucoma, urinary alkalinization (cystinuria), metabolic alkalosis, altitude sickness tox: hyperchloremia metabolic acidosis, neuropathy, NH3 tox, sulfa allergy |
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Loop diuretics
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Furosemide, Torsemide
Sulfa loop diuretic inhibits cotransport of Na/K/2Cl in thick ascending loop prevents concentration of urine by abolishing hypertonicity of medulla LOOPS LOSE Ca use: edematous states, HTN, hyperCa Tox: Ototox, nephrotox, hypoK, dehydration, gout, sulfa allergy |
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Ethacrynic acid
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loop diuretic that is NOT a sulfa
Phenoxyacetic acid derivative |
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Loop diuretics
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Furosemide, Torsemide
Sulfa loop diuretic inhibits cotransport of Na/K/2Cl in thick ascending loop prevents concentration of urine by abolishing hypertonicity of medulla LOOPS LOSE Ca use: edematous states, HTN, hyperCa Tox: Ototox, nephrotox, hypoK, dehydration, gout, sulfa allergy |
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HCTZ
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inhibits NaCl reabsorption in early distal tubule
reducing diluting capacity of nephron decrease Ca excretion use: HTN, CHF, hypercalciuria, NDI tox: hypokalemic metabolic alkalosis; hypoNa hyperGLUC: glycemia, lipidemia, uricemia, calcemia sulfa allergy |
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Ethacrynic acid
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loop diuretic that is NOT a sulfa
Phenoxyacetic acid derivative |
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HCTZ
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inhibits NaCl reabsorption in early distal tubule
reducing diluting capacity of nephron decrease Ca excretion use: HTN, CHF, hypercalciuria, NDI tox: hypokalemic metabolic alkalosis; hypoNa hyperGLUC: glycemia, lipidemia, uricemia, calcemia sulfa allergy |
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K-sparing diuretics
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Spironolactone & Eplerenone
aldo receptor antagonists Triamterene & Amiloride Inhibit Na channel in DCT use: hyperaldo, K+ depletion, CHF tox: hyperK; spironolactone causes gynecomastia (anti-androgen effects); eplerenone does not have those effects (more specific action) |
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K-sparing diuretics
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Spironolactone & Eplerenone
aldo receptor antagonists Triamterene & Amiloride Inhibit Na channel in DCT use: hyperaldo, K+ depletion, CHF tox: hyperK; spironolactone causes gynecomastia (anti-androgen effects); eplerenone does not have those effects (more specific action) |
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ACEI
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use: HTN, CHF, diabetic renal disease
tox: Cough angioedema taste changes **first dose hypotension (so be careful if also on diuretics) teratogen (renal damage) rash hyperkalemia *avoid with bilateral renal artery stenosis bc will significantly decrease GFR |
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ACEI
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use: HTN, CHF, diabetic renal disease
tox: Cough angioedema taste changes **first dose hypotension (so be careful if also on diuretics) teratogen (renal damage) rash hyperkalemia *avoid with bilateral renal artery stenosis bc will significantly decrease GFR |
