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