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ACUTE RENAL FAILURE/CHRONIC KIDNEY DISEASE

Acute Renal Failure/Chronic Kidney Disease Dr.Rommel P. Tolentino 060809 Feedback: 1. Absorption of most water: proximal tubule 2. Function of thin ascending loop: impermeable to water and urea 3. Hematologic manifestation of CKD except: 4. Furosemide 5. Further compromise GFR with renal hypoperfusion except: Beta-blocker (ace inhibitor, angiotensin 2 receptor blockers, NSAID) 6. Calcium to tubules: intrarenal vasoconstriction 7. Absence of aldosterone (promote K excretion): hyperkalemia 8. Hematologic complication except: lymphocytosis 9. Osteitis fibrosa and osteomalacia can be prevented if Ca phosphorus: below 70 10. Management of anemia of CRF except: Corticosteroids Blood supply to kidneys: renal artery and vein Function of kidneys: 1. filtration Pressure forces h2o and dissolved substances from glomerular into bowmans capsule 125ml 2. Reabsoprtion 3. Excretion 4. Secretion Glomerulus Filtration Proximal tubule 65% reabsorbed of Na and water Loop of henle Involved in counter current mechanism Distal tubule Some Na filtered is reabsorbed Collecting duct Water reabsorbed in final concentrating operation Main function of the kidney: release of erythropoietin Angiotensin Metabolism of vitamin D to most active form Renal 1. 2. function Tests: Urinalysis Specific gravity: 1.015-1.020 Crude test for concentrating ability Specific gravity > 1.020 No further tests needed *check for urine osmolality BUN Normal value 8-11mmol/L Major end product of protein metabolism Filtered and reabsorbed throughout the nephron

Increases in: Renal failure Dehydration - catabolic states (sepsis, injury) - blood in GIT high protein diet *not all patients with elevated BUN have kidney failure Serum creatinine Normal value: 50-100mmol/L; 1mg% Liberated from the muscle at a constant rate of 1 mg/min and excreted at the same rate Primarily the result of 2 functions: o Muscle mass o Renal function *rhabdomyolysis inversely correlated to GFR high creatinine, low kidney function 4. 3. -

Creatinine clearance Estimated creatinine clearance 140-age x kg body wt / 72 x serum creatinine (mg/dL) Normal values: o males: 100-150ml/min o Females: 24hr creatinine clearance (ml/min) Urine crea(mg/dL) x vol of urine 24hr (ml)/ plasma crea(mg/dL) x 144o mins

5. Nuclear GFR/ renal scan

6. 7. Isotope IV CT Scan, helical CT scan Renogram Arteriogram Ultrasound guided biopsy Percutaneous needle biopsy

ACUTE RENAL FAILURE Rapid decline in renal function over hours or days with or without oliguria (400-500ml/day) Etiology Pre-renal (hypoperfusion failure) o Cardiovascular failure Pump failure AMI, cardiac tamponade Vascular pooling o Hypovolemia Renal o Acute tubular necrosis Nephrotoxic (aminoglycosides, radiocontrast dyes) Pregnancy related septic abortion uterine hemnorrhage) Primary renal Glomerulovascular GN, malignant HPN, embolism, thrombosis Interstitial drug induced

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ACUTE RENAL FAILURE/CHRONIC KIDNEY DISEASE

Intratubular

*hyperkalemia 2ndary metabolic induced hyperkalemia: give NaHCO3 Oliguric phase: o Infection o Nutriotion Hypercatabolic state 3,00 calories/day 1gm/kg/day protein o Absolute indication for dialysis Fluid overload Hyperkalemia Serum creatinine >1,000 umol/L Uremic manifestations 2. Diuretic phase / maintenance F&E imbalance Despite urine o Plasma creatinine may continue to rise o May need to continue dialysis 3. Recovery phase Renal function continue to improve 6-12 months Renal function may not be achieved 100% Concentrating ability last to recover

Post renal o Calculi o Tumors o Functional o Clots o Fibrosis o Surgical

Diagnostic assessment of ARF 1. History and Physical Examination 2. Renal Function Tests Urinalysis Pre-renal o Benign/inactive sediments Post-renal o Inactive o Incomplete obstruction 3. Fluid and diuretic challenge Distinguish bet pre-renal and renal arf Correct pre-renal causes o Fluid o blood products still indistinguishable o CVP o More fluid Monitor VS/hydration state o JVP/lungs Restore 1st intravascular volume Potent loop diuretic Dopamine infusion o Aggravate the condition Mannitol irreversible ARF urine flow isotonic solution (.9 saline) Radiologic techniques

Prognosis of ARF Recovery depends on: o D CHRONIC RENAL FAILURE Condn with pathologic renal dse leading to persistently diminished renal Occurs when so little renal fxn remin that renal replacement therapy is.. Clinical features All organs are affected Causes of CRF 1. Chronic GN 2. Chronic obstructive uropathy 3. Hypertensive nephrosclerosis *diabetic nephropathy MC cause of CRF Diagnostic Assessment of CRF History Previous renal disease Clinical examination Pallor Pigmentation Uremic breath Neuropathy Features of underlying disease

*Give 4.

Clinical Course of ATN 1. Oliguric phase/ initiation o Several hours up to 2-4weeks o More than 6weeks: suspect other causes o F&E balance Fluid overload Fluid restriction Acidosis Hyperkalemia Treatment for hyperkalemia Mild to moderate: serum potassium 5.05.8mmol/L o Cation resin Severe cases o Dialysis o Temporary measures Ca gluconate D50 water + insulin Sodium bicarbonate

Investigation Anemia: normocytic, normochromic Radiology KUB/ultrasound small kidneys

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ACUTE RENAL FAILURE/CHRONIC KIDNEY DISEASE

Exceptions: polycystic kidneys, DM kidneys, amyloidosis Skeletal survey osteitis fibrosa Kidney biopsy hyalinized o

Clinical Feature of CRF General Malaise Lethargy Irritability GI Anorexia N/V Fetor Gastroenteritis

Conservative management of CRF 1. Correct reversible factors CHF, hypovolemia Remove obstn Eradicate underlying infections Control BP Avoid nephrotoxic drugs 2. Maintain F&E balance Fluid: 2L/day Edema restrict Na intake: replace obligatory loss 100mmol/day *2gms/day *pinch of salt: 5gm Loop diuretic Acidosis Kussmals breathing Minimize rate of progression to terminal RF Preparation for Renal Replacement Therapy

Respiratory Dyspnea Pulmonary edema Skin Pruritus Pigmentation Uremic frost Pallor Echimosis

3. 4.

GenitoUrinary Nocturia Hematologic Anemia Bleeding tendencies Endo Hyperparathy Thyroid dysfxn

Musculoskeletal Growth failure Deformity Bone pain Myopathy Metabolic Malnourished Gout Stages of Renal Function Deterioration 1. Diminished renal reserve 2. Renal insufficiency Mild azotemia Impaired concentrating ability Some anemia 3. Renal failure Chronic and persistent abnormalities o Azotemia, nocturia 4. Uremic syndrome Pathogenesis of CRF Ca salts deposits Endothelial damage Immunologic injury