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Nephro Study Guide

Block 4. Nephro Study Guide. Hyponatremia. First rule out non-kidney problems: Pseudohyponatremia (high triglycerides in blood that “fools” sodium auto-analyzer into using larger volume for calculating Na concentration)

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Nephro Study Guide

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  1. Block 4 Nephro Study Guide

  2. Hyponatremia • First rule out non-kidney problems: • Pseudohyponatremia (high triglycerides in blood that “fools” sodium auto-analyzer into using larger volume for calculating Na concentration) • Elevated non-Na extracellular osmoles (hyperglycemia  osmotic shift of water out of cells). Serum osmolality will be high even though Na concentration is low. • Psychogenic polydipsia  renal dilution system overwhelmed

  3. Hyponatremia • Second, figure out if patient is hypovolemic, hypervolemic or euvolemic

  4. Hyponatremia • Hypovolemic: Lack NaCl and water but have more water than NaCl • Hemorrhage • GI loss • Diuretics • Decreased extracellular vol increased ADH (volume problem wins over osmolar problem) • Findings: Low urine Na, hypotension

  5. Hyponatremia • Hypervolemic – volume overload dilutes Na. Have excess Na and water, but more water than Na • CHF • Cirrhosis • Low effective circulating volume (but not low total body water)  ADH release • Findings: CHF/cirrhosis symptoms, low urine Na

  6. Hyponatremia • Euvolemic- increase in total body water, but only a little increase in extracellular volume (no edema) • SIADH (cancer, TB, CNS problem) – ADH from ectopic source • Increased ADH (from pituitary gland) • SSRIs • Hypothyroidism • Glucocorticoid deficiency (low cortisol  inc in CRH  inc in ADH (and ACTH) ) • Chronic renal failure (only when GFR <15) • Thiazide diuretics (act at diluting segment – prevention of dilution  loss of Na)

  7. Treatment of Hyponatremias • Hypovolemic – correct ECV volume deficit with isotonic saline • Hypervolemic – treat CHF/cirrhosis, restrict water intake to 1 L /day • Euvolemic– treat underlying problem • Furosemide if SIADH • Conivaptan – ADH Receptor antagonist • If severe hyponatremia (<120) (seizures, coma) • Restrict water • Hypertonic saline – must be more hypertonic than urine output otherwise it will worsen problem • Furosemide • Overcorrection  central pontinemyelinolysis (potentially fatal CNS lesion)

  8. Summary of Hyponatremia

  9. Acid Base Disorders • Know normal values: • pH = 7.4 • [H+] = 40 • PCO2 = 40 • [HCO3-] = 24

  10. Metabolic Acidosis • Anion gap = Na – Cl – HCo3- • Normal gap is 6-10 • Increased Anion Gap: • DR SLIME • Diabetes • Renal Failure (inability to excrete H+ and unmeasured anions) – gap does not occur early on in renal failure • Salicylate OD (aspirin) (note – increased acid is ketoacids and lactic acid, not salicylate) • Lactic Acidosis (due to shock or sepsis) • Isoniazide (INH) (TB medication) • Methanol ingestion (alcoholics mistake it for alcohol) • Ethylene glycol ingestion (antifreeze)

  11. Metabolic Acidosis • Normal anion gap (6-10): • Diarrhea • Renal Tubular Acidosis (RTA) • Early Renal Failure (lost ability to make sufficient amt of ammonium to excrete H+, but GFR isn’t low enough yet that you lost ability to get rid of other unmeasured anions)

  12. Urine Anion Gap • Used to distinguish between diarrhea and RTA causes of metabolic acidosis • Urine: Na – K – Cl = urine anion gap (actually a cation gap bc unmeasured anion is NH4+) • If diarrhea, have high levels of ammonium in urine (anion gap <0) • If Type 1 or Type 4 RTA, have low levels of ammonium in urine (anion gap >0)

  13. For every H+ kicked into the urine a new bicarb is put back into the blood (way the kidney deals with daily acid load.)

  14. Urinary Dipstick • Nitrites • Gram negative bacteria • False negative: Vit C, urine in bladder <4 hours, inc specific gravity, bacteria w/o reductase • Leukocytes • Granulocytes (neutrophils, eosinophils, basophils) • False negative: insufficient time, some cephalosporins, oxalate, inc specific gravity • Protein • Albumin only • Do sulfosalicylic Acid (SSA) test if you suspect proteinuria but dipstick is negative (detects all protein types) • False Positive: increaed urine pH, detergents, contrast

  15. Urinary Dipstick • pH • Best to measure urine collected with oil because it prevents CO2 from leaving • Used for stone and RTA evaluation • Blood • Intravascular hemolysis (free Hb) or Rhabdomyolysis (free Mb) • False negative: Vit C • False positive: bleach, bacterial peroxidase • Specific Gravity • Dipstick not affected by glucose or contrast • No “normal” range – depends on volume status

  16. Urinary Dipstick • Ketonuria • Only picks up acetoacetate (so won’t pick up alcohol ketoacidosis) • False negative: acetone, Beta hydroxybutyrate • Glucosuria • High blood glucose  spilling glucose • Or • Fanconi  decreased reabsorption of glucose • False negative: Vit C

  17. Urine Microscopy • Dysmorphic RBC • Glomerulonephritis • Renal tubular epithelial cells • Tubular injury. Big, fried egg appearance • WBCs • Interstitial nephritis (eosinophilsfrom allergic reaction) • Infection (UTI)

  18. Casts • Hyaline Casts • solidified Tamm-Horsfallmucoprotein secreted from the tubular epithelial cells of individual nephrons • Normal – especially in dehydrated states • Granular Casts (muddy brown) • ATN – tubular injury  cells shed into lumen and stick together • Broad, waxy casts • Heavy proteinuria. Non-specific. • May suggest very low urine flow associated with severe, longstanding chronic kidney disease • Bigger than hyaline casts • RBC Casts • Acute glomerulonephritis • Oval fat bodies / fatty casts • Nephrotic syndrome (hyperlipidemia) • If cholesterol or cholesterol esters are present, they are associated with the “Maltese cross” sign under polarized light • WBC Cast • Pyelonephritis, allergic interstitial nephritis or post strep glomerulonephritis Granular Cast - Coarse

  19. Crystals Uric acid crystals • Ca oxalate / phosphate • Most common (60-70%) • Struvite • 10-15% • Recurrent UTI hx • Urease producing • Uric Acid • 5-10% • Radiolucent on x-ray but can see on CT • Dissolve with oral meds • Tend to form in acidic urine • Cystine • Rare • genetic Struvite Crystals (Staghorn, coffin) Phosphorus, Magnesium, Ammonium

  20. Urolithiasis (kidney stone) • 10% lifetime risk • Men > women • 4th and 5th decade • Tx: • Observe – spontaneous passage • Oral dissolution • Flomax to dilate ureter (alpha blocker) • ESWL (extracorpeal shock wave therapy) • Endoscopic or open surgery

  21. Pyelonephritis • Routes of Infection • Blood • Lymphatic route • Ascending (vesicoureteral reflux) • Complicated UTI = UTI in pt. with functionally, metabolically or anatomically abnormal urinary tract • Risk factors for pyelonephritis after UTI • Male, pregnant, catheter, abnormal tract, recent Ab use, prolonged symptoms, DM, immunosuppression, inherited susceptibility

  22. Organisms • Uncomplicated • Gram Negative: • E. Coli (72%) • Klebsiella • Proteus • Other • Gram positive • Enterococcus (5%) • Other • Complicated • E. Coli (21-54%) • Klebsiella • Enterobacter • Citrobacter • Proteus mirabilis • Providencia • Pseudomonas aeroginosa • Entercoccus

  23. Diagnosis of UTI • Nitrite Test • Lots of false negatives but few false positives • Leukocyte esterase • 45-86% sensitive • Pyuria – treat for UTI empirically

  24. Treatment of UTI • Hydration (WBC don’t like urease so water helps dilute urine) • Analgesia • Culture if pregnant or if symptoms persist or return • Medications: • Uncomplicated: • 3 days fluoroquinolone or TMP/SMX or Nitrofurantoinor Fosfomycin • Diabetes patients: • 7 days fluroquinolone or TMP/SMX • Pregnancy: • 7 days cephalosporin or amoxicillin if susceptible (fluoro are teratogens) • Recurrent: • >2 UTI/yr – prophylaxis • 2 UTI/yr – patient initiated therapy (give Rx to use in future)

  25. Renal Cysts • Autosomal Dominant Polycystic Kidney Disease (ADPKD) • Adults • Mutation in APKD1 or APKD2 (Adult Polycystic Kidney Disease) – Chromosome 16 (90%), 4 • Multiple, large, bilateral cysts that ultimately destroy the kidney parenchyma • Symptoms: • Flank pain • Hematuria • HTN • Urinary infection • Progressive renal failure • Associated with • polycystic liver disease, • berry aneurysms • mitral valve prolapse • Colon diverticulitis (lecture)

  26. Renal Cysts • Autosomal Recessive Polycystic Kidney Disease (ARPKD) • Kids • Mutation in PKHD1 • Significant Renal Failure in utero can lead to Potter’s (morphogenesis of fetus from dec amniotic fluid) • 50% of neonates die from pulmonary hypoplasia (incomplete dev of lungs from oligohydramnios) • Concerns for those neonates who survive: • HTN • Portal HTN • ESRD (1/3)

  27. Renal Cysts • So Remember: • ADPKD – Adults • Adults are Dominant (dominatrix) • ARPKD – Kids • Kids like Recess!

  28. Consequences of Renal Failure • Na+/H2O retention  CHF, pulmonary HTN, HTN • Hyperkalemia  heart problems • Metabolic acidosis • Uremia (clinical syndrome marked by inc BUN and inc Cr) • Nausea and anorexia • Peridcarditis • Asterixis(tremor of wrist when extended) • Encephalopathy • Platelet dysfunction • Anemia(dec erythropoietin) • Renal Osteodystrophy • failure of Vit D hydroxylation  decCa reabsorption from gut, inc PO4  secondary hyperparathyroidism  activation of osteoclasts • Dyslipidemia (inc triglycerides) • Increased lipoprotein synthesis to maintain oncotic P after loss of albumin • Growth retardation and developmental delay in kids

  29. Interstitial Nephritis • Drug Induced • Antibiotics or NSAIDS • Infection – bacterial pyelonephritis

  30. Thrombotic Microangiopathies • HUS – Hemolytic uremic syndrome: • Hemolytic anemia • Acute renal failure • Thrombocytopenia

  31. Renal Cancer • Even small renal mass has 80% chance it’s renal cell carcinoma so don’t need to biopsy since it’s such high chance • Risk factors: • Smoking • VHL gene mutation (tumor suppressor) • Patients with VHL have other tumors – hemangioblastoma, pheochromocytoma • Pathology: • Cells are clear (mostly because of glycogen) • Origin is proximal tubule • Prominent vasculature because of inc VEGF for angiogenesis

  32. Renal Cancer • Symptoms: • Constitutional • Occult, intermittent hematuria • Associated with paraneoplastic syndromes, polycythemia, hypercalcemia, HTN and leukomoid reactions • Treatment: • Surgery – radical or partial • Prognosis • Malignant with high risk for metastasis (to lung or bone most often) • Good survival if early stage

  33. Obstructive Uropathy:Impairment in outflow of urine • Symptoms: • Poor force of stream • Hesitancy • Incomplete emptying • Need to strain • Causes: • BPH • Urethral stricture • Kidney stone

  34. Acute Tubular Necrosis • Most common form of acute renal failure • Causes: • Antibodies (aminoglycosides) • Heme pigments (blood transfusion mismatch) • Rhabdomyolysis (major muscle breakdown from trauma  myoglobin is toxic like Hb is  myoglobinuria) • Heavy metals • Radiocontrast • Key findings: “muddy brown” casts • Kidney can recover (usually within 2-3 weeks) but fatal if not treated Muddy brown casts

  35. Cholesterol Emboli Syndrome • Causes: • Anticoagulation • Arterial instrumentation • Trauma • Spontaneous • Clinical clues: • Distal vessel emboli • Dec in complements (don’t know mechanism) • Eosinophilia • See cholesterol clefts • May see LivedoReticularis (cutaneous finding) – lace-like purplish discoloration of lower extremities

  36. Glomerulonephritis • Both have nephritic and non-nephritic have proteinuria • Nephritic (+ RBC ) • Post infectious glomerulonephropathy • Post Strep – 3-6 wks after skin infection • Epithelial “humps” on BM, “lumpy bumpy” • IgA • Usually 1-2 days after start of non-specific URI or pharygitis • Asians • RPGN (see crescents) • Goodpastures (antibodies against GBM) • Vasculitis • Wegner’s (C-ANCA) • Micro polyangiitis (P-ANCA) • Churg Strauss • SLE • “wire looping”, subendothelial deposits • Membranoproliferativeglomerulonephropathy(Hep C) • Alport’s syndrome • Genetic (x-linked) • Type 4 collagen defect

  37. Glomerulonephritis • Non-nephritic (No RBC, not inflammatory) • Nephroticsydrome= >3.5 g proteinuria/24 hr, lipiduria, hyperlipidemia, edema • Diabetic Nephropathy • FSGS (idiopathic or secondary) • HIV, heroine • Membranous glomerulonephropathy (Hep B, gold, penicillin, lupus) • Minimal Change Disease (NSAIDS, malignancy – Hodgkin’s) • Amyloidosis • Pre-eclampsia

  38. Hypokalemia – causes • Shift of K into cells • metabolic alkalosis, tx of DKA with insulin, admin of Beta agonists which stimulate Na/K ATPase, periodic paralysis from cell membrane defect • Prolonged dietary K depletion • Diarrhea • Renal K losses • Diuretics (inc distal flow)and vol depletion stimulates aldo secretion • Osmotic diuresis (diabetic ketoacidosis) • Vomiting • not lost from gastric juices • Inc [HCO3-]  more negative lumen  more K excreted • Volume contraction  increase aldo • Primary hyperaldosteronism (tumor) • Administer non-reabsorbable anion (penicillin) • Type 1 and 2 RTA • Rare genetic mutations in Na pumps leading to diuresis

  39. Diagnosing Hypokalemia • Urine potassium levels • <15 = dietary depletion or diarrheal K loss (kidney holding onto K) • >60 = renal loss

  40. Treatment of hypokalemia • Oral K • IV K in emergency • Correct alkalosis (normal saline)

  41. Hyperkalemia causes • Pseudohyperkalemia • Shifting of K out of the cells • Metabolic acidosis, low insulin states (DKA), Beta blockers, hyperosmolal states (hyperglycemia – osmotic drag pulls water with K out of cell) • Damage to cells with K+ leakage into serum • Crush injury • Rhabdomyolysis • Tumor lysis after chemo • Massive hemolysis • Renal K retention • GFR <20 • K sparing diuretic • ACE/ARB • NSAIDS • Type 4 RTA • Hypoaldosteronism or adrenal insufficiency • Drug induced • Potassium supplements • ACE I and ARBs • Potassium sparing diuretics • Beta 2 blockers • NSAIDs

  42. Diagnosing Hyperkalemia • Clinical diagnosis (urine K not used)

  43. Treatment of Hyperkalemia • With normal EKG: • Tx. Underlying cause • Low K diet • Diuretics or Kayexalate • With EKG changes: • Membrane stabilizer: Ca • K shifting agents- activate Na/K ATPase – Beta agonists, insulin, bicarb • Diuretics – furosemide • GI Binding agents – Kayexalate – ion exchange resin that binds colonic K • Dialysis

  44. Secondary Hypertension • Renal parenchymal – most common • Kidney not filtering well so retaining water and get hypertensive • Diagnose with urinalysis, Cr • Drugs • Ephedra, ephedrine, cocaine, methamphetamine • Renal artery stenosis • Dx: Doppler US • Primary hyperaldosteronism • Dx: serum aldo: renin ratio >30:1 • Pheochromocytoma • Headache, palpitations, diaphoresis

  45. Metabolic Alkalosis • GI loss of H+ • If gastric juice is removed, no stimulus for pancreatic HCO3- secretion and no hydrogen ion pumped into the blood – net result – increase in plasma HCO3- • Renal loss of H+ • Hyperaldo (lumen more negbc of Na reasbsorption increased H+ secretion) • Hypokalemia – K moves out of the intercalated cell and H ions move into cell to maintain electroneutrality H gets pumped into urine  for every H pumped into urine a bicarb is pumped into blood • Diuretics (inc flow) • Hypokalemia  shift of H+ from plasma into cells • Admin of HCO3- • Contraction alkalosis • Extracellular fluid contracts around a constant amt of extracellular HCO3-

  46. Maintenance of Alkalosis • 1. Volume Depletion (can’t excrete bicarb as well and get increased aldo) • 2. Chloride Depletion – both diuretics and loss of gastric secretions deplete Cl (HCl or NaCl) • Cl enhances activity of H+ ATPase pump • Cl depletion stimulates renin secretion  incaldo • 3. Hypokalemia

  47. Dx and Tx of Alkalosis • Urine Chloride • <15 = vomiting, diuretic use (body reabsorbing Cl) • Tx: volume repletion with saline and KCl to allow H+ to move out of cells • >20 = hyperaldosteronism • Tx: remove adrenal tumor, acetazolamide • Saline Responsive: • Vomiting • Diuretics • Post-hypercapnia • Low Cl intake • Saline Resistant • Hyper aldo • Edematous Disorders

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