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Approach to Renal Disorders AIMGP Seminar Revised by Nick Hariton November 2006 Objectives To identify appropriate strategies for investigation of the patient with kidney disease To discuss interventions that may alter the course of disease To discuss indications for referral to a nephrologist Guidelines Elevated Serum creatinine: recommendations for management and referral. CMAJ 1999: 161:413-17 National Kidney Foundation: Kidney Disease Outcomes Quality Initiative (NKF-KDOQI), 2002 Practice guidelines for Chronic Kidney Disease. 2003. Annals of Internal medicine. Vol. 139 Number 2. Stages of Renal Failure Stages of Renal Failure GFR (cc/min) Stage 1 >90 Stage 2 (Mild) 60-90 Stage 3 (Moderate) 30-59 Stage 4 (Severe) 15-29 Stage 5 (End-stage) <15 Creatinine is an estimate of GFR Cockcroft-Gault: (140-age) x wt x 100 = GFR (cc/min) 72 x serum Cr GFR (females) = GFR (males) x 0.85 MDRD 24 hour urine for creatinine CASES: What is Considered an ELEVATED Creatinine? 55 yo 70 kg male with Cr of 220: GFR =37 moderate 75 yo 45kg female with Cr of 220: GFR = 16 severe 75 yo 45kg female with Cr of 85: GFR =40 moderate 75 yo 45kg female with Cr of 45: GFR =76 mild Workup of a decreased GFR Approach 1. Identify chronicity (Acute vs chronic) 2. Identify the cause, especially reversible causes 3. Identify Indications for Referral to a Nephrologist 4. Initiate a cause specific management plan in a multidisciplinary team. Acute vs Chronic Renal Failure ACUTE - Fever - Hypovolemia - Sepsis - New hypertension - Recent nephrotoxins - No hypocalcemia - No hyperphosphatemia - No anemia CHRONIC - previous confirmed nephropathy - Already diminished CrCl - Atrophic kidneys (<10cm on U/S) - Normochromic normocytic anemia - Hypocalcemia - Hyperphosphatemia Abdominal Imaging Normal size kidneys in chronic kidney disease Diabetes Polycystic kidney disease Myeloma Kidney Amyloidosis HIV Nephropathy Underlying Cause CHRONIC KIDNEY DISEASE PRE-RENAL RENAL POST-RENAL GLOMERULAR INTERSTITIAL VASCULAR Pre-Renal Disease Medications: Renal Artery Stenosis Decrease effective circulating volume NSAID Diuretic Congestive heart failure Cirrhosis Hypovolemia (losses or decreased intake) Normal urine sediment, decreased urine [na+], increased BUN:Cr Post-Renal Disease Intraluminal obstruction: Nephrolithiasis Luminal obstruction Transitional cell carcinoma Severe BPH Extraluminal obstruction Retroperitoneal fibrosis Lymphadenopathy (lymphoma) Mass Glomerular Disease Active Sediment (RBC casts, hematuria) IgA Nephropathy Post-infectious GN Autoimmune disease and vasculitis Chronic hepatitis and HIV Nephrotic Syndrome (bland sediment, >3g/day proteinuria) Primary and secondary causes DIABETES Interstitial Disease Polycystic Kidney Disease Chronic infectious pyelonephritis Allergic interstitial nephritis Autoimmune interstitial nephritis Reflux nephropathy Myeloma Kidney Vascular Disease Large-sized Arteries Renal artery stenosis Medium-sized Arteries HYPERTENSIVE NEPHROSCLEROSIS Vasculitis Arterioles Microangiopathies (scleroderma, HUS/TTP, cyclosporine) Venous thrombosis History and Physical Exam signs or symptoms of underlying disorder: i.e. volume status, flank pain, obstruction, diabetes, hypertension, vasculitis altered kidney function: urine output, urine discoloration, edema renal failure: anorexia, vomiting, altered mental status, HTN medications: NSAID, ACEI, analgesics, aminoglycosides, contrast, Chinese herbs Laboratory Investigations Required: Estimation of GFR Urinalysis Albumin:Creatinine Ratio Renal Imaging CBC, Electrolytes, Calcium, Phosphate, Bicarb, Albumin Potentially useful: 24-hour Urine protein Fasting Glucose Serum / Urine Protein Electrophoresis HIV and Hepatitis serology Autoimmune serologies MR Angiography UptoDate Renal Biopsy Should be considered: Ff noninvasive tests have failed to establish a diagnosis in a patient with: Nephrotic syndrome (except in DM or established amyloid) Non-nephrotic proteinuria if associated with renal dysfunction Lupus nephritis (for dx and staging) Acute nephritic syndrome Unexplained acute/ subacute renal failure To direct and evaluate effectiveness of therapy Management of Renal Disease Treatment of Reversible Causes Preventing or Slowing Progression Treating and Preventing the Complications Identifying Individuals Requiring Renal Replacement Therapy Slowing Progression Hypertension ACE inhibitors preferred because: More potent antiproteinuric effect, especially in nondiabetics Large body of evidence from RCTs (in diabetics and non-diabetics) RRR 30% for progression to ESRD Benefit persists in severe kidney disease Management of Complications Coronary artery disease Anemia Calcium and phosphate homeostasis Renal osteodystrophy Platelet dysfunction Fluid overload Acidosis and hyperkalemia Decreased drug clearance Referral to Nephrologist Late referral (< 12 months pre dialysis) is common Survey of Ontario Family MDs: 84% would not refer with creat 120-150 (>50% loss of GFR) 28% would not refer with creat 150-300 almost all would refer with creat>300 Consequences of referral shortly before dialysis: more complications longer hospitalization to initiate dialysis more difficulty with initiation of dialysis worse survival! Better outcomes with early multidisciplinary care CMAJ 1999: 161:413-17 Canadian Guidelines Renal replacement therapy is NOT rationed (i.e. everyone should be considered) Reversible causes should be sought at diagnosis At least 1 year is required to prepare for dialysis Refer, at the latest, at Cr clearance of 30 ml/min, or Cr of 300 But…there are probably not enough nephrologists/ clinics to meet this demand Adequate communication with the Nephrologist will allow proper stratification of patients CMAJ 1999: 161:413-17 For AIMGP Clinic It is reasonable to follow stable renal failure patients, and work up and manage appropriately Refer to nephrology when: Cr >300 or Cr clearance <30 ml/min Renal biopsy indicated Indicators of aggressive disease are present: Rapid decline in creatinine homeostatic derangement i.e. acidosis, volume overload, high K high protein excretion Difficult to control BP low HDL black race In Summary Appoach To Proteinuria Normal Protein Elimination: < 150mg / day protein < 30mg / day albumin Classification of Proteinuria Transient Orthostatic Persistant Glomerular barrier tubule • Normally, the larger proteins are excluded at the glomerular barrier • Smaller proteins can pass, but are mostly reabsorbed Mechanisms of Proteinuria Glomerular Dysfunction Leakage of large proteins through glomerular membrane and podocytes Transient (epinephrine and AII mediated) Fever Exercise Congestive Heart Failure Persistant Glomerular Disease Leaky Glomerular barrier tubule •Large proteins are able to pass by the abnormal glomerular barrier Mechanisms of Proteinuria Tubular Dysfunction Inability of renal tubules to reabsorb small filtered proteins Specific transporter dysfunction Eg Fanconi’s syndrome Generalized tubular dysfunction Progressive chronic renal failure Interstitial Disease tubule Malfunctioning tubules unable to reabsorb the smaller proteins filtered at the glomerulus Mechanisms of Proteinuria Increased filtered protein load Overwhelms ability of kidney to reabsorb protein Increased GFR (mild proteinuria) Pregnancy, fever Increased filtered protein Myeloma, MGUS Glomerular barrier tubule • Filtered load of proteins exceeds the tubular reabsorption rate (similar to glucosuria in hyperglycemia) Diagnostic Approach Step 1 Clinical Assessment (History and Physical) and examination of urinary sediment History: urinary symptoms, infections, rash, risk factors for HIV and hepatitis Pmhx: Cancer, CHF, HTN, CTD, DM FHx: Alports, Fabry’s Drugs: NSAIDS, Gold, Heroin Physical exam: vitals, JVP, peripheral edema, ascites, rash, joint swellings Diagnostic Approach Rule out transient proteinuria with repeat urinalysis: Fever, exercise, UTI In young patients (age < 30) perform a split urine collection (upright and supine) to exclude orthostatic proteinuria If the above investigations are negative - STOP Diagnostic Approach Persistant proteinuria not due to a known underlying cause (eg CHF or diabetes) requires further investigation for glomerular and interstitial disease: 24h urine for protein or urine albumin:creatinine ratio Serum creatinine and estimation of GFR CBC, electrolyes, Fasting blood sugar Serum and urine protein electrophoresis Serology: Hep B, Hep C, HIV, ASOT, VDRL ANA, Rheum factor, C3/C4, ANCA Renal Imaging (eg ultrasound) Malignancy screen Renal Biopsy Indications for renal biopsy: Diagnosis unclear and Persistant proteinuria with > 3g / day Increasing proteinuria Declining GFR Prognosis and management Eg staging SLE nephritis Summary Asymptomatic proteinuria is a common problem Initial investigations are targeted to rule out transient, self-limited conditions and benign orthostatic proteinuria Persistent proteinuria, particularly nephrotic range or associated with declining GFR, requires further investigation Conclusions When evaluating a patient with a renal disorder: Identify and treat reversible causes of renal failure Initiate management to slow the decline in renal function Manage coexisting conditions Have clear indications for when to refer to nephrology subspecialists Organize an approach to asymptomatic proteinuria