Presentation Transcript

1. Nephrology Board Review

2. Outline • Hypertension • Kidney in pregnancy • Clinical Evaluation of Kidney • AKI • CKD • Glomerulonephritis • Electrolytes

3. Outline • Hypernatremia,hyponatremia • Hypokalemia, hyperkalemia • Hypercalcemia, hypocalcemia • Nephrolithiasis • Genetic diseases of Kidney • Renal Replacement Modalities

4. JNC Stratification

6. Office Bp measurements • Use auscultatory method with properly calibrated and validated instrument • Patient should be seated for 5 minutes in a chair with feet rested on the floor and arm supported at chest level. • Appropriate size cuff should be used to ensure accuracy. • Atleast 2 measurements should be made. • We should provide written and verbal confirmation of bp numbers and goal

7. Ambulatory BP monitoring • ABPM is warranted for evaluation of “white coat HTN” in the absence of target organ injury. • ABPM values are lower than clinic settings. • Awake, individuals with HTN have an average value >135/85 mm Hg and during sleep >120/75mm Hg. • Bp drops by 10-20% during the night, and if not then it may signal CV disease. “Non Dippers”

8. Modification Approximate SBP reduction(range) Weight reduction 5–20mmHg/10 kg wt loss Adopt DASH Diet 8–14 mmHg Dietary NA reduction 2–8 mmHg Physical activity 4–9 mmHg Moderation of alcohol consumption 2–4 mmHg Lifestyle Modification

9. Causes of Secondary HTN • Renal disorders: parenchymal disease: GN, Nephrotic syndrome, PCKD, CKD; • Renovascular Disease • Endocrine Disorders: Pheo, Primary hyperaldosteronism, Cushings syndrome, Carcinoid, Hyperthyroid or hypothyroidism, Hyperparathyroidism, Acromegaly.

10. Secondary HTN • OSA • Polycythemia • Medications such as steroids, EPO, CSA, Prograf.. • Stimulants/drugs/etoh • Coarctation of Aorta, Liddle’s syndrome, Gordon’s syndrome, 11 Beta hydroxysteroid deficiency, Licorice, GRA

11. Laboratory Evaluation • Routine Tests • EKG • Urinalysis • Blood glucose and Hct • Serum Potassium, Creatnine and Calcium • Fasting Lipid profile • Optional Tests: urinary Albumin excretion • More extensive tests are not warranted unless BP Control is not achieved.

12. Principal Cell

14. Without Compelling Indications With Compelling Indications Drug(s) for the compelling indications Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed. Stage 1 Hypertension(SBP 140–159 or DBP 90–99 mmHg) Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination. Stage 2 Hypertension(SBP >160 or DBP >100 mmHg) 2-drug combination for most (usually thiazide-type diuretic and ACEI, or ARB, or BB, or CCB) Not at Goal Blood Pressure Optimize dosages or add additional drugs until goal blood pressure is achieved.Consider consultation with hypertension specialist. Algorithm for RX of Hypertension Lifestyle Modifications Not at Goal Blood Pressure (<140/90 mmHg) (<130/80 mmHg for those with diabetes or chronic kidney disease) Initial Drug Choices

15. Diuretics Ace Inhibitor ARB CCB Aldost Inhibitor Beta Blocker Compelling Indications

17. Differential Diagnosis of Azotemia • Etiologies of elevated Cr: • Kidney disease • Large Muscle mass, AA • Medications that block creatnine secretion cimetidine, trimethoprim, probenecid • Substances that interfere with creatnine assay- cefoxitin, flucytosine, acetoacetate, bilirubin

21. Acute Kidney Injury

22. Definition of Acute Kidney Injury • Loss of renal function measured as GFR over hours to days • Expressed clinically as the retention of nitrogenous waste products in the blood.

23. Definitions • Azotemia- accummulation of nitrogenous wastes • Uremia- symptomatic renal failure • Oliguria- urine output <400-500ml/24hrs • Anuria- urine output<100ml/24hrs

25. Causes of Anuria • Obstruction (vast majority of patients with anuria)Bilateral renal cortical necrosisFulminant glomerulonephritis (usually some type of rapidly progressive glomerulonephritis)Acute bilateral renal artery or vein occlusion (rare)

31. Classification of the Etiologies of AKI

33. Differential Diagnosis of Acute Renal Failure • Prerenal acute renal failure • True intravascular depletion Sepsis, hemorrhage, overdiuresis, poor fluid intake, vomiting, diarrhea • Decreased effective circulating volume to the kidneys Congestive heart failure, cirrhosis or hepatorenal syndrome, nephrotic syndrome • Impaired renal blood flow because of exogenous agents Angiotensin-converting enzyme inhibitors, nonsteroidal anti-inflammatory drugs, CSA. Hypercalcemia. Abdominal compartment syndrome with increased renal vein pressures

34. Diagnostic Criteria for HRS • Major criteria: Low GFR (<40ml/min or cr>1.5mg/dl) • Absence of shock, ongoing bacterial infection, treatment with nephrotoxins or volume loss • No improvement with diuretics or volume expansion with 1.5L of isotonic saline • Proteinuria<500mg/dl and no US evidence of obstruction or parenchymal dz.

35. Diagnostic Criteria for HRS • Minor criteria • Urine volume <500ml/day • UNa<10mmol/L • Urine osm>plasma osm • Urine rbc<50 per high power field • Serum sodium <130 mmol/L • Arroyo et al Hepatology 1996

36. AKI in Liver disease • Pre renal azotemia • HRS • ATN • Interstitial Nephritis • Glomerular syndromes: IGA, cryoglobulinemia, MPGN, Membranous Nephropathy

37. Precipitating factors for HRS • SBP • Severe Bacterial Infection • GI Bleed • Major surgery • Aggressive diuresis • Paracentesis

38. Abdominal Compartment Syndrome • Clinical setting Trauma patient following massive volume resuscitation, post liver tx, mechanical limitations to abd wall such as burn injuries, post surgery etc. Bowel obstruction or pancreatitis. Clinical manifestations include: respiratory compromise, decreased CO, intestinal ischemia, oliguric AKI

39. Abdominal Compartment Syndrome • Pathophysiology of AKI- Increased renal venous pressure, increased parenchymal pressure, decreased perfusion • Diagnosis- suspect in distended abdomen. Excluded if bladder pressure<10 and dx when bladder pressure >25mm Hg. • Treatment Abdominal decompression

40. Differential Diagnosis of Acute Renal Failure • Postrenal acute renal failure • Benign prostatic hypertrophy or prostate cancer, cervical cancer, retroperitoneal disorders, pelvic mass or invasive pelvic malignancy, intraluminal bladder mass (clot, tumor or fungus ball), neurogenic bladder, urethral strictures • intratubular obstruction (crystals or myeloma light chains),

42. Intrinsic AKI • ATN • AIN • AGN • Acute vascular syndromes • Intratubular obstruction

43. Acute Interstitial Nephritis • Acute Kidney injury due to lymphocytic infiltration of the interstitium • Classic triad fever rash and eosinophilia (described in the methicillin patients and occurrs <30% of cases)

44. Drug induced PCN Cephalosporins Sulfa Rifampin Phenytoin Furosemide NSAIDS PPI Ciprofloxacin Malignancy Idiopathic Infection related Bacterial Viral Rickettsial TB Systemic diseases SLE Sjogrens syndrome TINU Acute Interstitial Nephritis

45. Common Drugs That Can Cause Allergic Interstitial Nephritis • Allopurinol (Zyloprim) • Cephalosporins • Cimetidine (Tagamet) • Ciprofloxacin (Cipro) • Furosemide (Lasix) • Nonsteroidal anti-inflammatory drugs • Penicillins • Phenytoin (Dilantin) • Rifampin (Rifadin) • Sulfonamides • Thiazide diuretics

46. History Preceeding illness or drug exposure Physical exam Fever, rash Lab finding eosinophilia Urine findings Non nephrotic proteinuria Hematuria Pyuria Wbc casts eosinophiluria Acute Interstitial Nephritis

47. Acute Interstitial Nephritis • Pearls • NSAID AIN is often without urine eos. • 3 sets of urine without eos has a NPV of >95% for AIN (other than from NSAIDs) • Urine eos can be positive in pyelonephritis, GN, Radiation nephritis and AIN

48. Acute Interstitial Nephritis • Treatment • Discontinue offending drug • Steroid therapy may hasten recovery but no RCT only case cohorts.

50. Acute Glomerulonephritis RPGN- 3 types • Ab mediated against basement membrane. Anti GBM dz • Ag-Ab complex deposit in the GBM: SLE, HepC, post strep, post infectious, endocarditis associated, IGA • Pauci immune: Wegner’s, Microscopic polyangiitis, Churg strauss

Load More ...