ISSN:0002-9629    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Background:Diuretics are widely used and generally safe, but like any therapeutic agents, they may cause side effects.Methods:A review of recent literature pertaining to diuretic usage was performed, with emphasis on specific reports of side effects. Reports of large-scale hypertension trials employing diuretics were also examined for descriptions of diuretic-related complications.Results:All diuretics promote excretion of sodium. Depending upon the site and mode of action, some diuretics increase excretion of potassium, chloride, calcium, bicarbonate, or magnesium. Some can reduce renal excretion of electrolyte-free water, calcium, potassium, or protons. Consequently, electrolyte and acid-base disorders commonly accompany diuretic use. Except for the mildly natriuretic collecting duct agents, which are used mainly to limit potassium excretion, all diuretics can cause volume depletion with prerenal azotemia. Loop agents and distal convoluted tubule agents, such as the thiazides, produce hypokalemic, hypochloremic, metabolic alkalosis that responds to potassium chloride replacement. Carbonic anhydrase inhibitors produce less hypokalemia and volume depletion but commonly induce metabolic acidosis that is often symptomatic. The potassium-sparing agents also limit proton excretion, and spironolactone may produce metabolic acidosis. Hyperkalemia is a leading complication of the potassium-sparing agents, especially in patients with an underlying tendency for hyperkalemia. Thiazide diuretics, in particular, have been linked to glucose intolerance, which may be an effect of hypokalemia rather than the diuretic itself. Whether diuretic-induced hypokalemia increases cardiovascular risk is controversial. Loop agents and thiazides may lead to hyponatremia, which, in the case of thiazides, may cause permanent neurologic damage. Dose-related reversible or irreversible ototoxicity may complicate treatment with loop agents. Nephrocalcinosis, nephrolithiasis, hypomagnesemia, and hyperuricemia can potentially complicate treatment with some diuretic agents. Reported idiosyncratic reactions to diuretics include interstitial nephritis, noncardiogenic pulmonary edema, pancreatitis, and myalgias.Conclusions:Potential side effects of a diuretic can often be anticipated from its mode of action on the kidney. These complications may be mitigated with careful monitoring, dosage adjustment, and replacement of electrolyte losses. Other side effects are idiosyncratic and cannot be prevented.

ISSN:0002-9629    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Generalized edema results from alterations in renal sodium homeostasis that ultimately result in an expansion of extracellular fluid volume and accumulation of interstitial fluid. The common edematous disorders include congestive heart failure, cirrhosis, nephrotic syndrome, and renal insufficiency. The abnormalities of sodium homeostasis contributing to edema formation in each condition are discussed. Management of volume homeostasis, with an emphasis on the role of diuretic therapy, is reviewed.

ISSN:0002-9629    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

The diuretics in our therapeutic armamentarium have predictable effects based on their nephron sites of action. All but spironolactone must reach the lumen or urinary side of the nephron to exert their effects. Thus, in settings of decreased renal function, doses must be increased to deliver more diuretic into the urine. In other edematous disorders, such as congestive heart failure (CHF) and cirrhosis, adequate amounts of diuretic reach the site of action if renal function is satisfactory. Diminished response in these conditions is caused by a decrease in the sensitivity of the nephron to the diuretic, the mechanism of which is unknown. Rather than using large single doses of diuretic in CHF and cirrhosis, multiple doses and/or combinations of diuretics should be used. Therefore, thiazide diuretics coupled with loop diuretics are most logical because they affect different nephron sites and the thiazide counteracts distal nephron hypertrophy that may occur with loop diuretics alone. Ample studies have shown that such combinations can result in a truly synergistic response. Using pharmacokinetics and pharmacodynamics of diuretics, we can design therapeutic regimens in which satisfactory control of fluid and electrolyte homeostasis can be achieved in the vast majority of patients.

ISSN:0002-9629    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

A wealth of studies performed with a spectrum of methods spanning simple clearance studies to the molecular identification of ion transporters has increased our understanding of how approximately 1.7 kg of NaCl and 180 L of H2O are absorbed by renal tubules in man and how the urinary excretion is fine-tuned to meet homeostatic requirements. This review will summarize our current understanding. In the proximal nephron, approximately 60 to 70% of the filtered Na+and H2O is absorbed together with approximately 90% of the filtered HCO3−. The exact quantities are determined by many regulatory factors, such as glomerulotubular balance, angiotensin II, endothelin, sympathetic innervation, parathyroid hormone, dopamine, acid base status and others. The essential components of absorption are luminal membrane Na+/H+exchange and the basolateral (Na++ K+)-ATPase. In the thick ascending limb of the loop of Henle, 20 to 30% of the filtered NaCl is absorbed via Na+2Cl−K+cotransport driven by the basolateral (Na++ K+)-ATPase. No H2O is absorbed at this nephron site. The transport rate is determined by the Na+load and by several hormones and neurotransmitters, including prostaglandins, parathyroid hormone, glucagon, calcitonin, arginine vasopressin (AVP), and adrenaline. In the distal tubule, some 5 to 10% of the filtered load is absorbed via Na+Cl−cotransport in the luminal membrane driven by the basolateral (Na++ K+)-ATPase. The rate of transport is again determined by the delivered load and by several hormones and neurotransmitters. One of the tasks of the collecting duct is to control the absorption of approximately 10 to 15% of the filtered H2O, regulated by AVP, and just a few percent of the filtered Na+, controlled by aldosterone and natriuretic hormone. The water absorption proceeds through the luminal membrane via aquaporin 2 and through the basolateral membrane via aquaporin 3 channels and is driven by the osmotic gradient built up by the counter current concentrating system. The Na+absorption occurs via Na+channels present in the luminal membrane driven by the basolateral (Na++ K+)-ATPase. With no pharmacological interference, urinary excretion of Na+can vary between less than 0.1% and no more than 3% of the filtered load, and that of H2O can vary between 0.3 and 15%.

ISSN:0002-9629    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Overdose with calcium channel blockers (CCBs) may lead to serious complications. CCBs act by blocking calcium entry into the cell, thus lowering intracellular calcium ([Ca2+]i). [Ca2+]iduring CCB overdose has not yet been reported. We measured [Ca2+]iin lymphocytes of a patient with acute verapamil overdose with a complex clinical picture. A 59-year-old woman was admitted after a suicidal ingestion of 7200 mg of a sustained-release verapamil preparation. She presented with hypotension, complete atrioventricular block, stupor, hypokalemia, and hyperglycemia. Acute oliguric renal failure, acute pancreatitis, and the adult respiratory distress syndrome further complicated her medical course. Treatment was supportive and she recovered completely. Intracellular calcium ([Ca2+]i) was measured in the patient’s lymphocytes using a spectrofluorometer with the calcium-sensitive dye Fura-2-acetoxymethyl ester. Thirty nine hours after the ingestion, [Ca2+]iwas low at 52 nM (compared with 80 nM in a healthy control subject). Lymphocytic [Ca2+]idid not respond to stimulation with phytohemagglutinin (PHA). Fourteen days after the verapamil overdose, after the patient had recovered completely, lymphocytic [Ca2+]iwas still low at 55 nM. At this time, there was an incomplete response to PHA in the lymphocytes. Three months after the ingestion, [Ca2+]iwas normal, with a normal response to PHA. Verapamil overdose may run a complex clinical course, but full recovery is to be hoped for with full supportive care. Cellular intoxication, as reflected by low lymphocytic [Ca2+]i, is prolonged and lags behind the clinical recovery by weeks.

ISSN:0002-9629    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

A 62-year-old man with multiple nontender skin nodules is presented. Some of these nodules discharged a purulent looking fluid. At presentation, the patient did not have any other complaints. No infectious, neoplastic, or immunologic origin could be found for the nodular rash. Biochemical profile, imaging, and skin biopsy confirmed the diagnosis of disseminated fat necrosis (DFN) accompanying asymptomatic pancreatitis. The process involved the mesenteric, subcutaneous, and intramedullary fat. The skin lesions were surgically treated. Mesenteric and intramedullary fat necrosis were watched closely. A year later, the patient was readmitted with a diagnosis of pancreatitis. Subcutaneous and intramedullary necrosis were completely resolved at this time, and only mesenteric fat necrosis prevailed. The clinical syndrome of DFN, its etiology, pathophysiology, treatment, and prognosis are discussed.

ISSN:0002-9629    

出版商:OVID    

年代:2000

数据来源: OVID