By Edgar Lerma, Jeffrey Berns, Allen Nissenson
To-the-point diagnostic and healing info on kidney ailments, high blood pressure, and kidney transplantation
CURRENT necessities of Nephrology & high blood pressure is a realistic, cutting-edge evaluation of the medical administration of kidney illness and high blood pressure. Concise and authoritative, the publication bargains a constant, easy-to-follow presentation and carefully addresses high blood pressure and the entire spectrum of kidney diseases.
Conveniently provides one sickness according to page
Bulleted information overlaying necessities of prognosis, Differential analysis, and therapy for every affliction state
A Pearl, and generally, a reference for every condition
Every part or subsection prepared in alphabetical order
Important subspecialty issues, together with care of pediatric, aged, diabetic, aged, diabetic, and important care sufferers
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Low solute intake limits the renal ability to excrete water independent of antidiuretic hormone. Differential Diagnosis Primary polydipsia seen in patients with psychiatric disorders or with lesions affecting the thirst center in the hypothalamus. • Low solute intake seen in malnourished states like excessive beer drinkers (beer potomania). • Correction phase of hyponatremia due to other causes. • ■ Treatment • • ■ Primary polydipsia is treated with water restriction. Low-solute-intake hyponatremia is treated by increasing solute intake.
Mineralocorticoid receptor antagonist (spironolactone, epleronone) or amiloride for idiopathic hyperaldosteronism. Pearl Stop beta blockers, ACE inhibitors, and angiotensin receptor blockers before screening with aldosterone/plasma rennin activity ratio. Reference Ganguly A: Primary aldosteronism. N Engl J Med 1998;339:1828. 34 Current Essentials: Nephrology & Hypertension Secondary Hyperaldosteronism ■ Essentials of Diagnosis • • • • • ■ Differential Diagnosis • • • • • • ■ High plasma aldosterone levels and volume expansion with hypertension associated with elevated renin.
In cases of potassium shift into intracellular compartment, the urinary potassium excretion can be variable. • ■ Differential Diagnosis Intracellular shift: alkalosis, increase uptake (hyperalimentation, leukemia, insulin), and familial periodic paralysis. • GI losses: nasogastric suction, diarrhea, villous adenoma, laxative abuse, and ureterosigmoidostomy. • Skin losses in perspiration. • Decreased intake: starvation, tea-and-toast diet, and anorexia nervosa. • ■ Treatment Treat or eliminate reversible causes.