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Renal Failure


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
Created by: Adam Barnard Adam Barnard