[A clinic for prevention of progression of kidney failure]. / Eine Klinik zur Prävention des Fortschreitens der Niereninsuffizienz.

Prevention in nephrology is only possible with the cooperation of patients and their families. The nurse plays a considerable role in working with patients and is a major player in the team, responsible for follow-up of the patient, where the earliest interventions can help delay and sometimes avoid dialysis. The hypertension clinic is the beginning of a continuum until dialysis. This paper describes three clinics that are managed in the renal service and indicates how they contribute to offering optimal care to a renal population.

Hemodynamic and renal effects of the protein kinase inhibitor staurosporine in conscious rats.

To evaluate the pattern of hemodynamic responses produced by an inhibitor of protein kinase C (PKC), staurosporine 0.03-0.55 mg/kg was administered intravenously (i.v.) to conscious, normotensive rats chronically instrumented with vascular catheters for direct measurement of blood pressure (BP) and i.v. administration of drugs and either an aortic flow probe for measurement of cardiac output (CO) or miniaturized pulsed Doppler flow probes for measurement of hindquarter, renal, and mesenteric vascular resistances. Staurosporine decreased mean arterial pressure (MAP) and total peripheral resistance (TPR) and increased heart rate (HR) in a dose-dependent manner. Because staurosporine decreased resistance in all three vascular beds monitored (hindquarter, renal, and mesenteric), staurosporine is probably a nonselective vasodilator that decreases MAP by decreasing resistance in a number of peripheral vascular beds. Staurosporine produced biphasic effects on CO, dF/dtmax and peak aortic blood flow; these parameters were significantly increased at doses less than 0.3 mg/kg and decreased to levels equal to or significantly less than control values at doses greater than 0.3 mg/kg. In comparison, the calcium channel blocker nitrendipine decreased MAP and TPR and increased HR, CO, dF/dtmax, and peak aortic flow in a dose-dependent manner over the entire dose range (0.01-1 mg/kg i.v.). Staurosporine (0.3 mg/kg) and nitrendipine (1 mg/kg) produced similar changes in MAP (-44 +/- 3 and -33 +/- 2 mm Hg, respectively), yet staurosporine affected dF/dtmax to a lesser extent than nitrendipine (-5 +/- 36 and 390 +/- 46 ml/s/s, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Natriuretic and vasodilating activities of intrarenally administered atriopeptin II, substance P and bradykinin in the dog.

The mechanism of the diuretic effect of atrial natriuretic factor is unclear. In this study, we compared the renal vasodilating and diuretic effects of renal arterial infusions of rat atriopeptin II in anesthetized dogs to see if natriuresis and increases in total renal blood flow were associated. The vasodilators substance P and bradykinin also were tested. Volume (V), Na+ and K+ concentration and Na+ and K+ content (UNaV; UkV) of urine from the infused and contralateral kidneys (IK; CK) were measured as well as mean total renal blood flow (RBF) of the IK. Atriopeptin II (30-1000 ng/kg/min) slightly promoted RBF by up to 20%, but raised V, UNaV and UkV by a maximum of 79, 190 and 100%, respectively. Substance P (0.01-30 ng/kg/min) raised RBF of IK by a maximum of 59%, reduced mean blood pressure by 26% and had a biphasic effect on IK excretion: V, UNaV and UkV were increased maximally by 105, 154 and 42% at 1.0 ng/kg/min, whereas progressively less diuresis, natriuresis and kaliuresis occurred at higher (hypotensive) doses. CK excretion was unchanged. Bradykinin (1-100 ng/kg/min) raised RBF, V, UNaV, and UkV of IKs by a mean maximum of 97, 70, 201 and 47%, respectively, with no changes in mean blood pressure or CK excretion. The natriuretic and hyperemic effects of nonhypotensive doses of each peptide were significantly correlated. However, atriopeptin II uniquely promoted Na+ excretion, but not RBF at the lowest dose tested, and, after 10 min washout of the 1000-ng/kg/min dose, and did not appreciably promote RBF after 10 min of infusion. It also caused CK diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Potassium-sparing effect of trilostane in hydrochlorothiazide-treated rats and dogs.

Trilostane, which inhibits three beta-hydroxysteroid dehydrogenase and aldosterone synthesis in rats and monkeys, significantly attenuated the oral potassium-wasting effect of hydrochlorothiazide (HCTZ) in rats and dogs when coadministered with the diuretic. The steroid reduced the kaliuretic and enhanced the natriuretic (and hyperreninemic) activity of HCTZ in rats, thereby promoting the urinary sodium/potassium ratio. Trilostane completely prevented HCTZ-induced hypokalemia in dogs and tended to reduce the degree of secondary aldosteronism. The combination also promoted hematocrit of dogs by 8% and decreased serum Na+ concentration by 7 meq/liter. When administered alone, trilostane increased canine serum potassium levels slightly and promoted rat urinary Na+/K+ ratio. Results confirm previous reports of antikaliuretic activity of trilostane in diuretic-treated rats. Further, the data indicate that frank hypokalemia induced in dogs by hydrochlorothiazide can be prevented by adjunctive trilostane therapy without eliciting hyperkalemia.