Potassium Disorders N Ganesh Yadlapalli, MD Professor of Medicine University of Cincinnati College of Medicine

K+ Balance Intake: dietary and parenteral Urinary excretion (90%) Regulated mainly by aldosterone GI loss (10%) Inc’d with CKD

Potassium Distribution ECF 80 -100 mEq ICF About 4000 mEq Saltwater extracellular is not K

Body Weight of 90 Kg Intra Cellular Fluid 40 Liters K+ 150 mEq/L Extra Cellular Fluid -- 20 Liters K + 4.5 mEq/L Total K + = 100 mEq Plasma K + 4.5 mEq/L

Intra cellular Fluid 40 Liters K + 150 mEq/L Extra Cellular Fluid -- 20 Liters ( 100 mEq of K) PO intake 40 mEq of of K + Total K + = 100 + 40 K + Na K + increases from 4.5 to 6.5 mEq/L Plasma K + 6.5 mEq/L

Potassium Balance Insulin Catecholamine pH Intra cellular Fluid 40 Liters K + 151 mEq/L Extra Cellular Fluid -- 20 Liters PO intake of 40 mEq K+ Total K + = 100 Inc in intracellular Potassium K + K + Na K + dec’s from 6.5 to 4.5 mEq/L Plasma K + 4.5 mEq/L Potassium Balance

Potassium Balance Insulin Catecholamine pH Intra cellular Fluid 40 Liters K + 151 mEq/L Extra Cellular Fluid -- 20 Liters PO intake of 40 mEq K+ Total K + = 100 K + K + Increase in intracellular Potassium Na + K + decreases from 6.5 to 4.5 mEq/L Plasma Potassium Balance K + 4.5 mEq/L Urinary Excretion GI excretion

Potassium levels back to normal Intra cellular Fluid 40 Liters K + 150 mEq/L Extra Cellular Fluid -- 20 Liters Potassium levels back to normal Total K + = 100 K + Na + K + 4.5 mEq/L Normalization of intracellular Potassium Plasma K + 4.5 mEq/L Urinary Excretion GI excretion

Intra cellular Fluid 40 Liters K + 150 mEq/L Extra Cellular Fluid -- 20 Liters Total K + = 100 K + Na + K + 4.5 mEq/L Normalization of intracellular Potassium Plasma K + 4.5 mEq/L

Causes of Hyperkalemia Inc’d Dietary Intake Dec’d Urinary Excretion Dec’d GFR Aldosterone deficiency Adrenal insufficiency ACE inhibitors ( dec aldosterone) Hyporeninemic hypoaldosteronism Diabetic nephropathy Aldosterone resistance Potassium sparing diuretics Internal Redistribution IC to EC shift Acidosis Exercise Cell Lysis Rhabdomyolysis Tumor lysis syndrome

Question 1 50yoM PMHx uncontrolled DM, had routine blood tests. His laboratory tests revealed serum creatinine 1.3 mg/dl, glucose 130 mg/dl, potassium 5.8 mEq/l, and a non-anion gap metabolic acidosis with serum HCO3 of 19 mEq/l. His BP control is chlorthalidone, lisinopril and amlodipine.

Question 1 Which of the following is the likely dx of his hyperkalemia and metabolic acidosis? CKD Lisinopril Type 4 RTA Increased intake D – Inc’d intake

Hyperkalemia Clinical Features Muscle weakness Cardiac effects- No clear correlation between serum potassium level and EKG changes Presence of hemodynamic instability indicates medical emergency

TTKG Gradient of K between tubular lumen at collecting tubule level and interstitial space TTKG < 3 indicate kidney is not wasting K+ > 7 indicate renal wasting U[K+] UOsm TTKG =  P[K+] POsm U[K+]  POsm = P[K+]  UOsm

Tx of Hyperkalemia Intra cellular Fluid 40 Liters K + 150 mEq/L Extra Cellular Fluid -- 20 Liters PO intake or IV Potassium Hyperkalemia K + Na + To shift K from EC to IC compartment with Plasma Insulin Catecholamine Bicarbonate Hyperkalemia Urinary Excretion GI excretion

Question 2 Give oral or rectal sodium polystyrene sulfonate 45yoF cc significant weakness. His potassium level is 6.5 mEq/L. ECG showed peaked T waves, but BP is stable. Which of the following statement is true regarding the mgmt ? Give oral or rectal sodium polystyrene sulfonate Sodium bicarbonate, 50-mL IV push and repeat K Patient is stable and tx can safely wait for repeat labs In addition to K depleting measures, give calcium gluconate D – lower K and give calcium gluconate

Question 3 All of the following drugs cause shift in potassium from extracellular to intracellular space except ? Inhaled albuterol IV Sodium bicarbonate Sodium polystyrene sulfonate IV Insulin with Dextrose C – sodium polystyrne sulfonate does not shift K ECF to ICF.

Hyperkalemia Protect heart from high EC potassium levels, if EKG abNMLities present CaCl or Ca gluconate (10 ml of 10% solution) Protects the conduction system from the effects of high K No effect on potassium levels

Potassium Shift From EC to IC Insulin with Glucose Rapid or slow infusion of Insulin with dextrose Action starts within 10 to 20 minutes 2 agonist Inhaled or IV albuterol Less predictable compared to Insulin IV Bicarbonate Alkalosis causes K shift into cells

Reducing Total Body K+ Loop diuretics Mineralocorticoid Inc’s renal potassium loss It can be combined with thiazide diuretics For acute cases, use IV doses of furosemide or bumetanide Mineralocorticoid Fludrocortisone 0.1 – 0.3 mg PO once a day For mgmt of chronic hyperkalemia ex. type IV RTA

Reducing Total Body K+ To inc GI excretion Sodium polystyrene sulfonate (Kayexalate) Exchanges K+ for Na+ in the colon Is given with sorbitol (by mouth) 15-30 g and repeat the dose as needed Use of sorbitol is associated with bowel necrosis. If the patient is NPO, give just kayexalate without sorbitol rectally Patiromer (Veltassa) Exchanges K+ for Ca+ in the colon Sodium free No reports of bowel necrosis Avoid taking medication for 3 hours after taking medication Dialysis Most effective, but limited to patients with renal failure

Question 4 45yoF cc kidney stone, PMHx generalized weakness, muscle pain, vomiting, joint pains. Dx of SLE was entertained, not confirmed, because of MSK symptoms and positive ANA. Physical examination was unremarkable except in pain secondary to kidney stone. . Laboratory test showed potassium of 2.6 mEq/l, non-anion gap metabolic acidosis with HCO3 of 15 mEq/l, and random urine pH of 7.0. CT scan of the abdomen revealed bilateral nephrocalcinosis.

Question 4 Which of the following is the likely cause of her clinical & laboratory presentation? Type 4 RTA Type 1 RTA Type 2 RTA Vomiting B – type 1 RTA

Hypokalemia Serum Potassium < 3.5 mEq/l Causes: Poor PO intake Redistribution into cells Inc’d loss Renal Non-renal

Laboratory Renal potassium wasting: if Non-renal potassium wasting Urine potassium loss > 20 mmol/ 24-hour a spot urine K+ > 15 mmol per liter Non-renal potassium wasting Urine K+ < 20 mmol / 24-hour period a spot urine <15 mmol per liter

Pseudohypokalemia Inc’d uptake of potassium by metabolically active cells in a blood sample laboratory artifact that may occur when blood samples remain in warm conditions for several hours before processing

Potassium Re-distribution Hypokalemic periodic paralysis Alkalosis Catecholamines, insulin, B2 agonist Barium

Hypokalemia with HTN High aldosterone and high renin: Malignant HTN, renal artery stenosis and renin secreting tumor. b. High aldosterone and low renin: Primary hyperaldosteronism, adenoma Idiopathic hyperaldosteronism Glucocorticoid remediable dz <1% and Carcinoma <1% c. Low aldosterone and low renin: Cushing's syndrome (high cortisone levels), Liddle Syndrome, Apparent Mineralocorticoid Excess, licorice ingestion (low cortisone levels)

HypoK Tx Degree of K + deficit depends on size of intracellular compartment ~200-400 mEq/L of K+ deficit in pts with serum K+ 3.5-3.0 ~400-800 mEq of K+ deficit in pts w/ plasma K+ from 3-2.0 mEq/L.

Pearls >95% of total body potassium is present intracellularly Potassium balance is maintained mainly by urinary excretion (90%) which is primarily regulated by aldosterone In patients with CKD, GI excretion plays an important role in K+ excretion Symptoms of hyperkalemia are usually nonspecific Presence of ECG changes in hyperkalemia is an emergency, and requires tx with IV calcium gluconate Goals are: to shift K from EC to IC compartment and deplete body K+ by inc’ing GI and renal excretion Barium toxicity causes acute hypokalemia Renal potassium wasting: if urine potassium loss > 20 mmol/ 24-hour, > 15 mmol/l on a spot urine sample in a hypokalemic person. Highlight Points: Do not wait for laboratory values to initiate treatment for patient with suspected Hyperkalemia based on ECG or PE