低钾血症 一、钾的生理2、肾脏的调节血钾在肾小球自由滤过约50-55% 在近端肾小管重吸收约30-35% 在髓袢重吸收远端小管和集合管泌钾二、引起低钾血症的原因Insufficient potassium intake: Deficient dietary intake Transcellular shift of K (no depletion): 三、低钾血症的诊断思路Barium poisoning 抑制钾在集合管管腔侧的传导Thyrotoxic periodic paralysis 作用在细胞的Na －K-ATPase 上，促进能量代谢和物质代谢引起严重的恶心、呕吐，最终导致电解质紊乱低镁血症40 ％的低镁血症患者伴有低钾血症原发性钾缺失时，肌肉的细胞内镁缺失而无低镁血症* *  K+ Balance Diagram Lungs Intercellular Intracellular Kidneys Lost in urine Plasma Normal Values: Major Functions: Mouth Stomach Small Intestine Large Intestine Lost in Feces Ingested Lost in sweat K+ 3.5-5.0 mEq /L Maintains intracellular osmolarity , controls resting potential of nerve and muscle, exchanged for H+ to correct pH, exchanged for Na+ when distal tubules reabsorb Na+  Passive diffusion Active transport Filtered into glomerulus , depending on blood pressure and GFR Secreted by aldosterone-controlled Na+/K+ ATPase in distal tubule Na+/K+ ATPase activated by insulin, epinephrine; inhibited by digitalis, beta blockers Passive diffusion K+/H+ exchange Repolarization (exercise, seizures) Reabsorbed in proximal tubule and loop of Henle  K+/H+ exchange K+  3.5-5.5 mEq/L, Total: 60 mEq  K+ channel Na+ K+ K+ Na+ Na-K ATPase Na-K ATPase  + + + + + + + _  _  _  _  _  _  _  K+ Distribution of potassium K+  150 mEq/L, Total: 4000 mEq 1、Factors that modify transcellular K+ distribution （钾的肾外调节）Catecholamine -adrenergic / -adrenergic  Pancreatic hormone  Insulin/Glucagon Acid-base status  Blood PH( Acidosis/alkalosis )  Plasma HCO3- ( Low/high ) Modifying factors Alkalosis Glucagon  Acidosis a- adrenergic Insulin b-adrenergic  CELL K+ Potassium Homeostasis Renal Handling of K+ in PCT K+ (Paracellular route) K+ Cl- X- Reabsorption of Sodium Chloride —Lessons from the Chloride Channels, NEJM,2004,350(13):1282 Renal Handling of K+ in TAL CaSR K reabsorption by H-K exchanger in intercalated cells K secretion by Na-K exchanger in Principal cells Renal Handling of K+ in DCT and CT Hypokalaemic periodic paralysis  Thyrotoxic periodic paralysis  Barium poisoning  Alkalosis  Insulin excess Potassium depletion: Extra-renal losses:  (1) Diarrhea  (2) Rectal villous adenoma  (3) Fistulas, Ureterosigmoidostomy  (4) Laxative abuse Renal losses:  (1) Excessive mineralocorticoids (primary& secondary aldosteronism, licorice ，ingestion, glucocorticoid excess)  (2) Renal tubular diseases (RTAs,leukaemia, Liddle’s syndrome,antibiotics, carbonic anhydrase inhibitors)  (3) Diuretics  (4) Magnesium depletion  Differential Diagnosis of Hypokalemia Hypokalemia Metabolic alkalosis Hypertension GI wasting Y N Urine K Urine Cl Insufficent intake Intracellular transition RTA N High Low High Plasma renin Laxatives Renal wasting Diuretics Bartter/Gitelman syn Urine Ca/Cr Diuretics RAS Renin secret Cushing syn Plasma Aldo Hyperaldosteronism Y High High Normal Low Low Congenital adrenal hyperplasia Chronic liguorice ingestion Apparent mineralocorticoid excess Liddle’s syn Carbenoxolone High Low Bartter’s syn Gitelman’s syn Insulin -adrenergic hyperthyroidism Periodic Hypok- alemic Paralysis 低血钾测尿钾尿钾正常高尿钾摄入少或吸收不良胃肠道丢失测PH 碱中毒不定酸中毒测尿氯<20mmol/L >20mmol/L 测血压正常高血压测Ald 高低低肾素高肾素低肾素正常或高肾素肾间质－小管疾病、低血镁、锂盐肾小管酸中毒、糖尿病酸中毒、乙酰唑胺呕吐、腹泻、高碳酸血症原醛利尿药、Batter 或Gitelman 、低血钾软病肾素瘤、肾动脉狭窄、恶性高血压Liddle 、CAH Cushing 、ACTH 分泌过多Thank you ！* * *