Renal
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| Associated with edema (w/w Na retention), ascites, HTN, ortho hypotn, skin striae, retinal sheen, renal vein thrombosis = | nephrotic syndrome
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| Total body water (TBW): compartments | 60% ICF, 40% ECF (32% ISV, 8% IVV)
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| Renal cell cancer etiology | smoking; hereditary (von Hippel-Lindau, papillary renal ca); HD/PD is RF
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| Called the "internist's tumor" = | Renal cell ca (spectrum of presenting s/s)
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| Renal cell cancer classic triad = | gross hematuria, flank pain, palpable mass
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| Furman grade is sued to stage: | Renal cell ca (I - III)
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| Painless hematuria, flank pain, palpable mass | Renal cell carcinoma
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| Crush injury, alcoholic on ground, elevated CPK, ARF = | Rhabdomyolysis
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| Oliguria, hematuria, proteinuria following streptococcal infection; AM facial edema & PM LE edema | Acute glomeruloneprhitis
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| Hematuria, purpuric rash following streptococcal infection | Glomerulonephritis, HSP
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| Kidney & lung bleeding (hematuria, hemoptysis) | Goodpasture syndrome
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| Hearing loss or tinnitus w/ metabolic acidosis | Aspirin OD (eg of AIN)
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| Nephrotic syndrome complications: | Pneumococcal PNA / cellulitis. Spontaneous bacterial peritonitis. PE. NOT cardiac arrhythmias
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| Infrarenal cause of ARF in a hospitalized patient | ATN
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| Infrarenal ARF pathophysiology | Vascular, glomerular, interstitial, tubular (ischemic), nephrotoxic, sepsis
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| Medications that can cause ATN | IV contrast, aminoglycoside, cyclosporines
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| ARF Sx/Sx | N/V/D, anorexia, GIB, asterixis; AMS, seizures, edema, rash, pruritus, purpura
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| CKD etiology | Glomerulopathies (diabetic nephropathy 40%), vascular (HTN 33%), tubulointerstitial nephritis (med sensitivity), hereditary (PKD), obstructive (eg, prostate dz)
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| Glomerulonephritis etiology | PSGS, Hep, Wegener, Goodpasture, Churg Strauss
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| Nephritic syndrome | AKI, HTN, urinary sediment (RBC, RBC casts)
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| Nephritic syndrome DDx | PSG, SLE, SBE, IgA nephropathy, HSP, Wegener
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| Nephrotic syndrome etiology | Peds: MCD. Adults: DM2, multiple myeloma, amyloid, SLE, PSGN, Hep C (membranoproliferative), HIV
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| CKD most common causes | DM, HTN, glomerulonephritis, PKD
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| CKD s/s | cachexia, pallor, HTN, ecchymosis, sensory deficits, asterixis, kussmaul
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| Causes of glomerulonephritis | HSP, post-infxs GN, IgA nephropathy, membranoproliferative GN
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| glomerulonephritis: focal vs diffuse | focal involves <50% of all glomeruli
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| Oliguria = | output <400 cc/day (or 0.5-1.0 cc/kg/hr)
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| In prerenal ARF (40-80% of all ARF), ineffective circulating volumes may be due to: | Sepsis (early); Anaphylaxis; 3rd space sequestration (pancreatitis, peritonitis, ischemic bowel)
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| Renal ARF: glomerular causes | Post-infective glomerulonephritis (GAS, after 1-3 wks; pneumococcus, staph); SLE; Vasculitis; H-S purpura
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| Renal ARF: vascular causes | Thrombosis; TTP/ DIC; NSAID OD; Severe HTN; HUS
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| Renal ARF: tx | LD dopamine; Mannitol in early rhabdomyolysis; Dialysis
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| Types of Intrinsic ARF (50% of all ARF) | ATN (85%), AIN (acute interstitial nephritis), AGN (acute glomerulonephritis)
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| Postrenal (5-10% of ARF) cause | obstruction
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| ARF patho | abrupt decrease in GFR -> retention of nitrogenous wastes
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| ATN sx/sx | weight loss
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| ATN mgmt | Diuresis, correct lyte disorders, low protein diet (prevent catabolism), improve perfusion if ischemic, ?ultrafiltration in CHF
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| AIN mgmt | supportive measures, remove causative agent, corticosteroids, ST HD
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| AGN mgmt | High-dose corticosteroids, cytotoxic agents, and/or plasmapheresis
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| Manifestations of CKD often do not appear until: | 40% of renal fn is lost (labs) and 80% is lost (clinical sxs)
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| CKD stage 1 = | slight kidney damage, GFR >90
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| CKD stage 2 = | mild, GFR 60-89
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| CKD stage 3 = | moderate, GFR 30-59
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| CKD stage 4 = | severe, GFR 15-29
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| CKD stage 5 = | kidney failure, GFR <15 or on dialysis
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| HD is generally started when: | serum Cr >8mg/dL or GFR <10
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| Survival rates for kidney transplant | 1 & 3-year rates for cadaveric organ transplant: 90% & 78%. For live donor transplant: 95% & 88%
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| ATN etio | Ischemia, nephrotoxins -> tubular injury: kidneys unable to concentrate urine & reabsorb Na
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| Medications that can cause AIN | NSAIDs (70%), Abx (PCN, ceph, sulfa, rifampin), diuretics, PPI, allopurinol, cimetidine, phenytoin, Cox-2, cisplatin
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| Endogenous nephrotoxins that can cause ATN | myoglobulins (eg, in rhabdo), uric acid (in leukemias & lymphomas), Bence-Jones proteins (in multiple myeloma), Hbg (in hemolysis)
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| 3 phases of ATN | Injury; maintenance (oliguric <500mL/day or non-oliguric, better prognosis), 1-3 weeks; recovery
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| ATN mortality | 20-50% (to 70% in pts with underlying comorbidities)
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| AGN patho | Glomerular inflammation -> damage to glomerular basement membrane (GBM) +/- mesangium & capillary endothelium. Secondary inflammatory agents become involved
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| Edema, HTN, hematuria with RBC casts = | nephritic syndrome
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| Sudden onset of cola urine, edema, oliguria, HTN = | PSGN
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| Most common form of AGN in world = | IgA nephropathy (Buerger dz): kids & young adults.
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| IgA nephropathy sx/sx | macro hematuria, URI (in 50%), GI sxs, flu-like illness; HTN & edema uncommon
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| HSP sx/sx | palpable LE purpura (2/2 leukocytoclastic vasculitis), arthralgias, N/V & colic melena
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| Small vessel ANCA-associated vasculitis = | Pauci-immune GN
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| Nephritic syndrome mgmt | Na/fluid restriction, diuretics, ?HD, tx HTN, immunosuppressives for inflammation. Abx PRN.
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| IgA nephropathy mgmt | ACEI / ARBs, corticosteroids, transplant PRN
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| Pauci-immune GN mgmt | corticosteroids and cytotoxic agents (cyclophosphamide); ?plasmapheresis
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| Anti-GBM GN mgmt | plasmapheresis, corticosteroids, cytotoxic agents
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| Cryoglobulin-associated GN mgmt | Tx underlying infxn. ?plasmapheresis, corticosteroids, cytotoxic agents. + Interferon-alpha in hep C infxn
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| Idiopathic nephrotic syndrome may be due to: | MCD, focal glomerular sclerosis, membranous nephropathy (AA: FSGN), membranoproliferative glomerulonephropathy
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| MCD is usually associated with: | allergies, Hodgkin dz, NSAIDs
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| Focal & segmental glomerulosclerosis (FSGS) is associated with: | heroin use, HIV, reflux nephropathy, obesity
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| Seen with IgM and C3 sclerotic lesions: | FSGS
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| Membranous nephropathy is associated with: | NHL, carcinoma, gold therapy, penicillamine, SLE
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| Seen with thickened GBM, granular IgG and C3: | Membranous nephropathy
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| Associated with URI and seen wtih granular C3, C1q, C4, IgG, IgM: | Type 1 membranoproliferative GN
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| Seen with Ce deposits only: | Type 2 membranoproliferative GN
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| May see thrombosis in nephrotic syndrome due to: | loss of protein C & S and antithrombin III
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| Nephrotic syndrome mgmt | Limit dietary salt & protein (0.6-0.8g/kg/day), match protein loss with PO intake to avoid malnutrition. ACEI. Statin. Thrombus PPx/Tx PRN
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| Choice of diuretics | Loops for fluid retention assoc w/pleural effusions / ascites. Metolazone may potentiate loop action. Thiazides in mild edema.
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| MCD mgmt | Prednisone 1mg/kg/day until a few weeks post remission (may take up to 16 weeks). Cyclophosphamide for recurrence.
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| Membranous nephropathy mgmt | Mild proteinuria: tx as w/nephrotic. Moderate (6-8 g/day): steroids and (chlorambucil or cyclophosphamide) x6 months
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| May recur after kidney transplant: | membranoproliferative glomerulonephropathy (50% cases progress to ESRD in 10 yrs, despite steroids & antiplatelet tx)
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| Infections that may cause AIN | Strep, Corynebacterium, Legionella, EBV, CMV, Mycoplasma, Rickettsiae, Toxo, Leptospirosis, Histoplasmosis
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| AIN patho | T lymphocytes (w/plasma cells & macrophages) -> cytotoxic interstitial damage -> inflammatory cell recruitment (ie, eosinophils)
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| Associated with bone marrow granulomas, chlamydia, mycoplasma, in women with wt loss / anemia / high ESR: | TINU (tubulointerstitial nephritis-uveitis)
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| Causes of Chronic Tubulointerstitial Nephritis (CTIN): | prolonged obstructive uropathy (most common), vesicoureteral reflux, analgesics, heavy metals
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| RTA types | I: classic distal. II: proximal. IV: hyporeninemic-hypoaldosteronemic
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| RTA type I labs | Urine pH >5.3; decreased K; increased Ca; stones
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| RTA type I etiology | decreased distal acidification
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| RTA type 2 labs | Urine pH variable; decreased K
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| RTA type 2 etiology | decreased bicarb reabsorption
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| RTA type 3 labs | Urine pH variable; INCREASED K+
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| RTA type 4 labs | Urine pH <5.3; normal K
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| RTA type 4 etiology | decreased aldosterone secretion
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| Diseases associated with P-ANCA | Churg-Strauss, polyarteritis nodosa
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| Disease associated with C-ANCA | Wegener
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| Disease associated with anti-GMB | Goodpasture (lung, kidneys, nephritic syndrome)
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