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Published byArnold Davis Modified over 10 years ago
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Acute Renal Failure A. Symptoms Polyuria, Oliguria or Anuria hematuria
Dysuria Uremia Definition: symptomatic azotemia Acidosis (± tachypnea) Mental Status changes Hypervolemia / Hypertension Hyperkalemia Pericarditis
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------------------------ Serum Cr x 72
Duration <3 months Oliguria <400 ml urine/24 hours Absolute increase Scr by 0.5 or 1.0 mg/dl or relative increase 25% Cockcroft – Gault Equation (140-age) x wt(kg) Serum Cr x 72
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B. Etiologies Location of Lesion Prerenal - ~70% of cases Intrinsic - ~25% of cases Post-renal (obstructive) - <5% of cases FeNa= urine Na x serum Cr X 100 serum Na x urine Cr Prerenal Renal (ATN) Urine Na <10 >10 FeNa <1% >1% response IVF good poor BUN/Scr >20 nl
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Decreased effective arterial volume
Pre-renal azotemia Decreased effective arterial volume CHF,,Cirrhosis,,Nephrotic syndrome,,Sepsis Renal Artery Stenosis (atherosclerosis, fibromuscular dysplasia) Cardiopulmonary bypass (>3 hours) Intravascular volume depletion GI loss…Vomiting..diarrhea…etc Renal loss diuretc..osmotic diuresis..etc Cutaneous loss hyperthermia..burns Hemorrhage Third space pancreatitis..severe hypoalbuminemia..cappillary leak
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II.Parenchymal Damage Nephritis (inflammation): glomerular vs. interstitial Tubular Injury: most common cause of ARF Nephrotic Syndrome (total protein losses) III. Obstruction of Outflow (~5%) Urinary Tract Infection (UTI) with Pyelonephritis Urinary Calculus disease (renal stones) Crystal Deposition Bladder tumors with extensive invasion Prostatic Enlargement: BPH vs. Carcinoma Unilateral obstruction with only one functioning kidney
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Vascular hypertension
Atherosclerotic (atheroembolism) - cholesterol emboli, 5-10% of hospitalized ARF Trauma Vasculitides Post-operative - aortic aneurysm repair, aortic cross-clamping Vasoconstricting Agents - NSAIDs, vasopressors
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Drug Induced ACE Inhibitors Radiocontrast Dye Interstitial Nephritis - sulfonamides, NSAIDS, other antibiotics Amphotericin Cis-Platinum Aminoglycosides Non-steroidal anti-inflammatory drugs (NSAIDs)
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Pathophysiology Ischemia is the underlying problem in ARF leads to depletion of cellular ATP and release of calcium Reactive oxygen species produced leading to further cell death Calcium release leads to phospholipase activation Neutrophils may mediate reperfusion injury (ICAM-1 is involved) Many nephrotoxins are renal vasocontrictors (eg. cyclosporine, radiocontrast)
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C. Initial Evaluation Consider possible etiologies and direct evaluation Medications should always be suspected Standard Blood Testing Electrolyte/renal panel, Ca2+, Phosphate, Mg2+, Albumin Complete Blood Count Foley catheter to rule out bladder obstruction
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Urine for electrolytes, dipstick and microscopic analysis
Osmolality, creatinine, Na+, K+, Cl- Urine spot protein to creatinine ratio (normal is <0.2) Pigment: Hemoglobin (myoglobin) Cells, Casts, Crystals, Organisms Consider Urine culture
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Renal/Pelvic Sono - stones, hydronephrosis, mass
Consider Abdominal radiograph if ultrasound is not done to rule out stones ESR, ASO titer, ANA, C3/C4 Anti-GBM Abs Renal Biopsy in rapidly progressing disease ANCA and Anti-GBM diseases - consider cyclophosphamide + glucocorticoids Idiopathic rapidly progressive glomerulonephritis often ANCA positive (other inflammatory diseases such as bacterial endocarditis can given ANCA+)
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Pathology Summary Glomerular Involvement Diffuse: all glomeruli in a section are diseased Focal: some glomeruli in a section are diseased Segmental: parts of individual glomerulus affected 2.Focal Glomerulonephritis: Some glomeruli are dead( necrosis, collapse, sclerosis b.Acute or chronic inflamation is often seen 3.Crescent Glomerulonephritis (very poor prognosis) Crescent (moon shaped) formation in glomerulus Affected glomeruli are non-functional
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Focal and Segmental Glomerulosclerosis: portions of many glomeruli are destroyed
5. Minimal Change Glomerulonephritis a. Glomeruli appear okay, but function is poor b. Electron microscopic evidence of basement membrane disease c. Response to glucocorticoids is usually very good 6. IgA Deposition a.IgA nephropathy b.Deposition of IgA immune complexes c.Differential includes Systemic Lupus (SLE) and Henoch-Schonlein Purpura (HSP)
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7. Proliferative Glomerulonephritis
a. Increase in mesangeal cell number b. Usually follows insults (eg. Post-Streptococcal) May be seen in collagen vascular disease, SLE 8. Collapsing Glomerulonephritis Major form seen in HIV nephropathy Usually late stage Rapid progression to renal failure (weeks-months) No effective therapy to date
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9. Tubular Necrosis a. Tubular cells die and slough off basement membrane b. The dead tubular cells form casts which can occlude lumen c. Glomular basement membrane may also be damaged
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E. Management Renal Diet Low phosphate, potassium, sodium, and protein High calcium and vitamin D Various multivitamin formulas available for renal patients, eg. Nephrovit® Low protein diet may slow progression slightly in chronic renal disease Phosphate and Calcium Dangerous if product of Calcium and Phosphage > ~70 (mg/dl) (will lead to precipitation)
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If product is close to 70, then phosphate should be lowered with aluminum compounds
These compounds should be given with meals to bind the phosphate directly If product is <60, then calcium should be given mg po tid with meals If calcium is low but phosphate normal, then calcium should be given before meals Consider using 1,25 dihyroxyvitamin D supplements
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1. Acidosis Renal tublar acidosis (RTA) is common in early renal failure Oral bicitra (citrate replaces bicarbonate) may be used Bicitra is contraindicated in edematous states due to high sodium content 2. Hyperuricemia Check uric acid levels Uric acid deposition in renal tubules may worsen progression of renal failure Allopurinol may be given ( mg po qd) to attempt normalization of uric acid
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3. Hypertension a. ACE inhibitors generally contraindicated in moderate to severe renal failure Calcium blockers such as nifedipine Labetolol is also very effective but patient should have LV EF>50% and no bronchospasm d. Consider Hydralazine for afterload reduction e. Pure alpha-adrenergic blocking agents may be effective, but tachyphylaxis may occur Diuretic improve hypertension/ volume overload
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4. Volume overload a. Attempt to maximize cardiac output and improve intravascular volume b. Diuretics often worsen renal failure but may be necessary to prevent pulmonary edema c. In general, potassium sparing diuretics should be avoided (high risk hyperkalemia) e. Dopamine or mannitol can be tried, but are usually not effective f. Albumin infusions are probably not helpful, but may help diuresis in low albumin states g. Dialysis may be required particularly in severe volume overload situations
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5. Protein Load Reducing protein load is thought to reduce azotemia Appears to slow progression of CRF Patients with moderate renal disease - some decrease in progression on low protein diet Patients with severe renal disease show no benefit on low protein diet 6. Hospital inpatients with ARF ~50% mortality rate
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7. Newer Agents Atrial natriuretic factor (ANF)= dilators + diuretic ANF (Auriculin®) ? efficacy in oliguric ARF ANF may increase renal dysfunction in diabetics receiving radiocontrast Brain derived natriuretic factor (BDNF) may be effective some patients Other vasodilators (eg. calcium channel blockers) are not effective Investigation renal growth/regeneration factors
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8. Dialysis Indications Serum abnormalities unresponsive to medical therapy Severe Acidosis Severe Hyperkalemia II Uremia Mental status changes (usually delirium) Nausea and vomiting Pericarditis (pericardial friction rub)
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III Volume Overload Hemofiltration or hemodialysis can be used to allow recovery of kidney after ARF Average duration of need for these therapies was 9 days in ARF After this time, kidneys regain function and increase urine output Native kidneys may continue with minimal function for 6-12 months of hemodialysis After that, native kidneys usually shut down permanently
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Kidney Transplantation
Excellent (and improving) results with cadaveric grafts. Living Related Donor kidneys superior to CRT New kidney usually placed in extraperitoneally in the pelvis Cyclosporin ,Prednisone, OKT3, mycophenolic acid, FK506 immunosuppression Combined Kidney Pancreas transplant in Diabetic ESRD patients
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