more DDA VP being available at site oe renal action, Cf the weU known enzyme inducer might be responsible for the possible inhibition of metabolism of DDAVP (Nies 1974).
Paradoxical hypertonie glucose-induced hyperkalemia has been described recently in two patients suffering from both diabetes mellitus and hyporeninernie seleetive hypoaldosteronism by GoIdIarb, Strunk, Singer andGoldberg (1975, 1976). Hyperosmolality seeondary to hypematrernia also induced significant hyperkalernia in diabetie neprhopathy (Rado). It was postulated by Goldlarb et aL (1975Goldlarb et aL ( , 1976) that in eombined aldosterone-insulin deficieney there is adefeet in the reversion of the transfer of potassium to extracellular fluid whieh norrnally oeeurs after infusions of hypertonie solutions. Therefore in the present work we have investigated the effeets of a pharrnaeologieal dose of aldosterone, cortisone and synthetie ACTH on the hypertonie sodium chloride indueed hyperkalemia in a nondiabetie, non-hypoaldosteronemie patient with stable ehronie renal failure and permanent baseline hyperkalernia not responsive to both bicarbonate and mineraloeortieoid therapy.In a 53-year-old man, narrowed renal funetions (serum creatinine 4.05 rng%, NPN 56 mg%, Ytterbium l69 -EDTA clearance 16 mI/min, 12SJ-hippuran elearance 59 mI/min) and tubular acidosis (urine pH 6.2 when blood pH 7.29; deereased titratable acidity) were found to be caused by ehronie interstitial nephritis with exeessive homogenous acidophil basal membrane thiekening encireling the eortical distal and colleeting tubules. Serum potassium (K) was 6.26 ± 0.13 mEq/L (n = 21), arterial blood pH was 7.25 ± 0.012 (n = 11) and arterial plasma bicarbonate was 15.14 ± 0.66 rnEq/L (n = 11). After prolonged peroral a11ca1i treatment the Iatter values were significantly increased to 7.361 ± 0.005 (n = 12; P < 0.01) and 20.98 ± 0.70 rnEq/L (n = 12; P < 0.001) resp., but K did not change (5.99 ± 0.38 rnEq/L; n = 20; NS). During 5 day treatment with aldosterone-acetate (5-10 rng A1docorten, CIBA-Geigy per day in divided doses intravenously) K was 6.56 ± 0.34 mEq/L (n = 5), and during a 3 day treatment with DOCA (3 x 10 rng per day intravenously) it was 6.93 ± 0.22 mEq/L (n = 3).Plasma cortisol deterrnined by the Mattingly's method was at 8 a.rn. 25-30 ug% and 6 hours after 2 mg Synaethen-Depot it was 100 ug%. (In 9 normal subjeets it increased from 20.8 ± 2.4 "g% to 68 ± 5.4 "g%). Urinary aldosterone excretion was (baseline) 19 J.IS per 24 hours (normal: up to 12 "g per 24 hours). Blood glucose was 110 mg% and the standard peroral GTT was normal. The solt loading protoeol consisted of fJVe 1 hour periods with urine eollections and blood sampling at the end of certain periods. After the fast (contro!) period 1 liter 2.5 % NaO solution was infused intravenously during the seeond hour. This protoeol was repeated after pretreatment with A. 6 eng aldosterone on the previous day with another 1 rng in the infusion bottle; B. 4 mg Synaethen-Depot Lm. andC 400 mg peroral cortison-acetate (Adreson, Organon) (B. and C. also pven on the previous day). The main results are depieted in the Figure. It can be seen that hyperosmotie loading in-SERUM 160 N. HIO (mEq/Ll 140 K (mE...
The mechanism of the decrease in plasma potassium induced by phosphate treatment was investigated in a 24-year-old hypertensive patient with hypophosphatemic osteomalacia, who was the youngest of four patients, belonging to a 23 number kindred of five generations. Parameters of potassium, sodium, calcium, and phosphate metabolism as well as specific renal functions have been studied in the basal state and during administration of graded doses of phosphate (500-6000 mg). Progressive hypokalemia developed during phosphate treatment. An inverse correlation was found between plasma potassium and doses of phosphate (plasma potassium = -0.2 g phosphate + 3.9 r = -0.49; p < 0.05; N = 21). A renal route of potassium loss was suspected, but could not be confirmed as potassium excretion did not increase although sodium excretion was augmented [basal sodium output: 56.7 mmol/24 h; phosphate treatment: 153 mmol/24 h (p < 0.05)]. Transtubular potassium gradient (TTKG) also decreased and an inverse correlation was found between TTKG and doses of phosphate (r = -0.37; p < 0.02; N = 38). Decrease of TTKG was possibly the result of suppressed K+ secretion. It was concluded that potassium loss occurred by a non-renal (intestinal) route in phosphate-induced hypokalemia. Although major hazards of treatment of hypophosphatemic osteomalacia with phosphate and calcitriol are secondary hyperparathyroidism and vitamin D intoxication, potassium loss also should be kept in mind.
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