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  1. Renal Board Review Brenda Shinar, MD

  2. Question 1. • Answer: A: Combinaton drug therapy

  3. Manage Newly Diagnosed Stage 2 Hypertension

  4. Untreated stage 1 hypertension with onset at age 35 will decrease a person’s lifespan by 16 years!

  5. Question 2. • Answer: D: Repeat blood pressure measurement

  6. Identify the cause of a patient’s change in blood pressure

  7. Question 3. • Answer: D: No change in management

  8. Manage HTN in a patient who is over age 80.

  9. Question 4. • Answer: D: Obtain a plasma aldosterone-plasma renin activity ratio

  10. Understand the differential diagnosis of resistant hypertension Definition: • Blood pressure measurements consistently exceed goal on 3 antihypertensive medications, one of which is a diuretic • BP controlled on > or = to four medications • 12.8% of adults being treated for HTN • Non-adherence to therapy • White coat resistant hypertension • Renal parenchymal disease • Renal artery stenosis • Pheochromocytoma • Primary hyperaldosteronism • OSAS • Drug- induced • Volume overload

  11. Primary Hyperaldosteronism:60% of patients have NORMAL K level • ALDOSTERONE HIGH • RENIN LOW • AR RATIO >25 is suggestive BUT NOT diagnostic • Metabolic alkalosis and hypokalemia MAY OR MAY NOT be present • 8 AM draw • OFF spironolactone or eplerenone for 6 weeks • Possibly off ACEI • NO CONFIRM test needed: • Spontaneous hypokalemia • Undetectable renin level • Aldosterone >30 ng/dL

  12. Question 5. • Answer: D: Type B lactic acidosis

  13. Diagnose type B lactic acidosis Type A Lactic Acidosis Type B Lactic Acidosis Normal systemic perfusion Impaired cellular metabolism or regional ischemia Metformin Linezolid (IV, prolonged) HIV medications Liver disease Malignancy D-lactic acidosis • Tissue hypoperfusion due to shock • Reduced systolic blood pressure may be minimized by severe vasoconstriction • Altered mental status • Cool extremities • Oligoanuria • Lactic acid level predicts mortality

  14. Question 6. • Answer: C: Urine chloride level

  15. Evaluate a Patient withHypokalemic Metabolic Alkalosis Chloride Responsive 90% Chloride UN-responsive 10% Hypertensive Hypervolemic ABNORMAL increase in aldosteroneor renin Distal tubule wastes H+ and K+ to hold onto Na+ Urine chloride HIGH >15 • Vomiting, Low effective circulating volume • Volume depleted • NORMAL increase in renin, angiotensin, aldosterone • Distal tubule wastes H+ and K+ and hold onto Na+ • Urine chloride LOW <15 • Cannot replace K until volume is replaced

  16. Question 7. • Answer: B: Estimate GFR using the Chronic Kidney Disease-Epidemiology Collaboration equation (CKD-Epi)

  17. Estimate the glomerular filtration rate in a low-risk, healthy person Equations 24 hour measurement Extremes in age Extremes in weight Pregnancy Cirrhosis Amputations Radionuclide Scanning Most precise method Used for kidney donor eval if GFR is borderline • Preferred to estimate GFR • Creatinine MUST be stable for 24-48 hours • MDRD (Modification of Diet in Renal Disease) • CKD-EPI (Chronic Kidney Disease Epidemiology) • Cockcroft-Gault

  18. Question 8. • Answer: B: Hypokalemic distal (type 1) renal tubular acidosis

  19. Diagnose hypokalemic distal (type 1) renal tubular acidosis

  20. Question 9. • Answer: B: Chlorthalidone

  21. Manage hypercalciuria in a patient with nephrolithiasis • Hypercalciuria: • >300 mg/24 hr MEN • >250 mg/24 hr WOMEN • >200 mg/24 hr BOTH • WORSENED by: • High sodium diet • High animal protein diet • Loop diuretics • DO NOT advise a calcium restricted diet, as this increases GI absorption of oxalate, increasing oxaluria • DO ADVISE: • Thiazide diuretic • Fluids > 2 liters/day

  22. Question 10. • Answer: C: Split urine collection

  23. Orthostatic proteinuria: • Uncommon over age 30 • (2-5 % of adolescents) • <1-2 grams per day • Supine collection is NORMAL • BENIGN condition

  24. Question 11. • Answer: D: Serum and Urine Electrophoresis

  25. Diagnose Multiple Myeloma as a cause of acute kidney injury Clinical Features of MM: Renal Complications: Tubular Damage Adult Fanconi’s syndrome RTA Proximal Type 2 Cast Nephropathy * Proteinaceous casts clog the tubules resulting in tubule atrophy Glomerulopathy Light chain disease deposition Resulting in albuminuria! Exquisite sensitivity to IV contrast! • Anemia (NCNC) (80%) • Bone pain (70%) • Recurrent infections • 25% presenting • 75% during disease • Renal complications (50%) • Hypercalcemia (25%) • Renal failure (25%) *most common

  26. Question 12. • Answer: A: Acute interstitial nephritis

  27. Diagnose Acute (Allergic) Interstitial Nephritis DRUGS: Antibiotics (B-lactam) NSAIDS * (nephroticproteinuria) with minimal change disease on biopsy Thiazides Proton Pump Inhibitors Phenytoin Allopurinol • Idiosyncratic drug-induced hypersensitivity • Fever, rash, eosinophilia, and elevated creatinine (10%) • UA: WBC, WBC casts • Eosinophiluria • NEGATIVE CULTURE (sterile pyuria) • < 2 gm/ 24 hr proteinuria

  28. Question 13. • Answer: B: IgA nephropathy

  29. Diagnose IgA nephropathy:The most common cause of nephritic syndrome Ig A Nephropathy (25-30%) Post-Strep Gnitis(4-8%) 7-10 days AFTERpharyngitis Antibodies to: Streptolysin O DNAse B Low complements (C3) DIFFERENTIAL (LOW C3): Lupus nephritis (20-30%) MembranoproliferativeGnitis (MPGN) (6-10%) • CONCOMMITANT pharyngitis • Normal complements DIFFERENTIAL (NL C3): • Pauci-immune glomerulonephritis (15-25%) • Anti-GBM antibody disease (3%)

  30. Question 14. • Answer E: Supportive Care

  31. Manage Post-Infectious Glomerulonephritis (PIGN) • MANY bacteria, viruses and parasites can cause PIGN • Most common nephritogenic strains of strep and staph • Rapid onset of hypertension, oliguria, erythrocyte casts, and edema, LOW C3 MANAGEMENT is SUPPORTIVE: • Early treatment of the bacterial infection • Diuretics for volume overload • Antihypertensives for elevated BP • Dialysis if necessary • NO evidence for immunosuppression, steroids, plasmapheresis

  32. Question 15. • Answer: A: Cryoglobulinemia associated with Hepatitis C

  33. Diagnose Hepatitis C virus associated glomerulonephritis • Occurs in up to 20% of patients with chronic Hepatitis C • Presents as membranoproliferativegnitis or mixed cryoglobulinemia (skin, kidney, and nerve involvement) • 1/3 relapsing dz with progression to ESRD • Low complement (C4) • + Rheumatoid factor • TREAT Hep C virus EXTRA-HEPATIC MANIFESTATIONS OF HEPATITIS C INFECTION: 1. MembranoproliferativeGNitis 2. Mixed Essential Cryoglobulinemia 3. Lichen Planus • (the 5 Ps) 4. PorphyriaCutaneaTarda • (vesicles, milia, photosensitivity)

  34. Question 16. • Answer: D: Pigment nephropathy

  35. Diagnose Pigment Nephropathy from Rhabdomyolysis • 2 types of pigment induced nephropathy: hemolysis or rhabdomyolysis • Urine dip + for blood with urine micro negative for red cells • Ischemia, blockage, or injury to tubules • Associated lab abnormalities with rhabdo: • Elevated CK level, aldolase • Hyperkalemia, hyperuriciemia, hyperphosphatemia, hypocalcemia • Treatment: • IV fluid, UOP 200-300/hour • Bicarbonate not proven • Dialysis not helpful unless indicated

  36. Question 17. • Answer A: Focal Segmental Glomerulosclerosis

  37. Diagnose Focal Segmental Glomerulosclerosis: the most common renal cause of nephroticsyndrome in US (36-80%) Primary Disease: Podocyte damage similar to minimal change dz Secondary Disease Associations: • Morbid obesity • Heroin use • HIV • Vesicoureteral reflux Risk factors for progression to ESRD: • Black race • >2 gm/24 hr proteinuria • Low GFR • BMI>27 • Hypertension Clinical Manifestations: Acute onset of nephrotic syndrome with hematuria, renal failure and hypertension in primary disease; Asymptomatic subnephrotic to nephroticproteinuria in secondary disease Management: Immunosuppression with steroids or calcineurin inhibitors in primary disease ACEI +/- ARB in primary and secondary disease BP goal < 125/75 mm Hg

  38. Question 18. • Answer: B: Membranous nephropathy

  39. Diagnose Membranous Nephropathy: the second most common renal cause of nephrotic syndrome Primary disease: Immune complexes of IgG react with antigens in the outer aspect of GBM Secondary disease associations: Malignancy Hep B and C NSAIDS Risk factors for progression to ESRD: Male gender Age>50 Persistent proteinuria > 4g/24 h over 6 months Declining GFR Clinical manifestations: Nephrotic syndrome with preserved GFR Renal vein thrombosis Management: ACE and/or ARB BP goal < 125/75 mm Hg Persistent proteinuria > 4g/24 hr cyclophosphamide, corticosteroids, or calcineurin inhibitor with possible need for rituxan

  40. Question 19. • Answer: B: 3% saline infusion

  41. Treat a patient who has symptomatic hyponatremia

  42. Question 20. • Answer: A: Chronic kidney disease and hypertension

  43. Diagnose underlying chronic kidney disease and hypertension in a pregnant patient Normal physiology in pregnancy Pearls in Pregnancy: Hypertension BEFORE 20th week indicates new dx of chronic hypertension Safe BP agents in pregnancy are methyldopa and labetalol: ACEI, ARBs and renin inhibitors are NOT safe Gestational hypertension develops AFTER 20 weeks: no proteinuria or end-organ damage Pre-eclampsiahypertension develops AFTER 20 weeks and is associated with proteinuria LOW dose aspirin reduces the risk of preeclampsia • Blood pressure lowers • Plasma volume increases • GFR increases • Renal pelvis, calices, and ureters dilate • Increased risk for pyelo • Hyperventilation causes resp alkalosis with increased renal bicarb excretion