Diagnosis of Hypokalemia Mahmoud Barazi, M.D. Nephrology Fellow TTUHSC

Case 77 y.o WF who presented with a chief complain of Diarrhea. Also found to have Hypokalemia and Hypomagnesaemia. HPI: - 7 days hx of diarrhea with decreased oral intake. - No F/C/S

Case PMH - Non-Hodgkin’s lyphoma S/P Autologus BMT - HTN - AKD - CHF

Case Home Medications: - ASA 81 mg daily - Lasix 20 mg daily - Robitussin 20 mEq p.o BID - Tylenol650 mg PO q4h prn - Folic Acid 1 mg po bid - Loratadine 10 mg po daily

Physical Exam VS: Tmp 99 HR 94 BP 101/51 RR 16 SaO2 92% Gen: A&O x 3, in mild distress HEENT: AT/NC, EOMI, PERRLA Neck: Supple, No JVD, No thyromegaly Chest: CTAB CVS: S1, S2 normal, No M/R/G, NSR ABD: Soft, NT, BS present, No organomegaly EXT: No C/C/E

presentation WBC6.2Hgb11.3Plt60 Na 137K 2.1Cl 95CO2 28 AG 16Glu 101BUN18Cr 1.1 Ca 7.8Alb 3.2Mg 1.4 UA pH 6.5Trace ProteinPositive Nitrite Moderated Leuk. EsteraseSpec Gravity 1.009CloudyRBC 0-3WBC 15-2 C-Diff neg. Urine culture was positive for E.coli

Causes of Hypokalemia Decreased K Intake Increased entry into cells -Elevation in pH -Increased Insulin -Elevated B-agonist activity -Hypokalemic periodic paralysis -Marked increase in blood cell production -Hypothermia -Chlorquine intoxication

Causes of Hypokalemia Increased GI losses -Vomiting -Diarrhea -Tube drainage -Laxative abuse

Causes of Hypokalemia Increased urinary losses - Diuretics - Primary mineralocorticoid excess - Loss of gastric secretions - Nonreabsorable anions - Metabolic acidosis - Hypomagnesaemia - Amphotericin B - Salt-wasting nephropathies – including Batter’s or Gitelman’s syndrome - Polyuria

Diagnosis of Hypokalemia Can usually be determined from the history In other case, the diagnosis is not readily apparent Measurement of BP, urinary K exertion and assessment of AB balance are often helpful

Urinary Response

Urinary response The minimum urine K concentration in response to Hypokalemia is 5 to 15 meq/L A normal subject can lower urinary potassium exertion below 25 to 30 meq per day in the presence of potassium depletion. < 15 meq per day is likely representative of extrarenal losses

Acid Base Assessment Metabolic Acidosis - with Low urine K exertion in asymptomatic patient is suggestive of Lower GI losses due to Laxative abuse or villous adenoma - with K wasting is most often due to DKA, Type 1 or Type 2 RTA

Acid Base Assessment Metabolic Alkalosis: -With low Urine K exertion is due to surreptitious vomiting or diuretic use -With K wasting and normal BP is most often due to surreptitious vomiting or diuretic use or to Batter’s syndrome. Urine pH and Urine Cl concentration are helpful -With K wasting and HTN is suggestive of surreptitious diuretic Rx in Pts with underlying HTN, renovascular disease or primary mineralocorticoid excess

Bartter’s & Gitelman’s Syndrome Autosomal recessive disorders Hypokalemia Metabolic Alkalosis Hyperreninemia Hyperplasia of juxtaglomular apparatus Hyperaldosteronism Occasionally hypomagnesaemia

Bartter’s Syndrome Named after Dr. Frederic Bartter Prevalence 1 per million Often, but not always associated with MR Pt with a variant of classic Bartter’s syndrome suffer from the same electrolytes disorders, but also has sensorineural deafness and renal failure

Gitelman’s Syndrome After Dr. Hillel Gitelman Prevalence is 1 per More benign than Bartter’s

Distinctions between Batter’s & Gitelman’s Syndrome Bartter’s SyndromeGitelman’s Syndrome Localization of defectAscending limb of HanleDistal Tubule Age of PresentationPrenatal, during infancy, early childhood Mostly late childhood or at adult age Biochemical differenceSerum Mg may be decreased Serum Mg is decreased Urinary exertion of Ca is increased Urinary exertion of Ca reduced Functional StudiesConcentrating capacity severely impaired Concentrating capacity normal or slightly impaired GFR may be normal or declining GFR is normal

Back to our Pt Day 4 of hospitalization Mg 1.6 K in 24 hour urine was 57 and Ca was 32 Day 9 of hospitalization Mg 1.8 K in 24 hour urine was 81 and Ca was 52

Diagnosis ?