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Trimethoprim-sulfamethoxazole is a frequently prescribed antibiotic with a wide spectrum of antimicrobial activity. A previously unreported and potentially lethal adverse reaction associated with "high dose" trimethoprim-sulfamethoxazole therapy, hyperkalemia, was described. Subsequent to the descriptions of hyperkalemia with "high dose" trimethoprim-sulfamethoxazole, a handful of cases noted the development of hyperkalemia with "standard dose" trimethoprim-sulfamethoxazole in elderly patients without evidence of an obvious defect in potassium homeostasis. A surveillance study of patients treated with "standard dose" trimethoprim-sulfamethoxazole as compared to similar controls treated with other antibiotics confirmed the rise in potassium associated with trimethoprim-sulfamethoxazole therapy. Recognition of this potassium disorder led to investigation and description of the mechanism by which trimethoprim-sulfamethoxazole-induced hyperkalemia. Trimethoprim was found to act like the potassium-sparing diuretic amiloride and reduce renal potassium excretion. Hence, trimethoprim-sulfamethoxazole therapy was found to be associated with a new adverse reaction, hyperkalemia, nearly 25 years after its introduction into clinical practice as an antimicrobial agent.

Secondary hypertension accounts for a minority of all cases of hypertension. Certain clues in the patient's medical history and laboratory parameters may help identify the rare patient with secondary hypertension. The association of hypertension with hypokalemia and renal potassium wasting should raise one's suspicion for a state of mineralocorticoid excess. The clinical syndrome of hypertension and hypokalemia may be related either to a high renin state, such as renovascular disease, or to a low renin state, such as primary hyperaldosteronism, adrenal enzyme defects, certain familial syndromes, and licorice ingestion. Over the past decade, a genetic basis has been identified for apparent mineralocorticoid excess (AME) syndrome, Liddle's syndrome, and glucocorticoid remediable aldosteronism (GRA). This brief review focuses on a few of the unusual conditions which cause a true or apparent mineralocorticoid excess state, and summarizes the clinical presentation, pathogenetic mechanism, and treatment of these diseases.

Lead intoxication in human beings has been documented since the second century B.C. Renal disease, hypertension, and gout have all been linked to lead by strong circumstantial evidence. Both acute and chronic nephropathy can occur as a result of lead poisoning. Acute renal failure develops following acute lead intoxication and is often associated with gastrointestinal, neurologic, and hematologic disorders. Both blood and urinary laboratory abnormalities are associated with acute intoxication and are often diagnostic. Chronic lead nephropathy, a chronic tubulointerstitial nephritis on biopsy, occurs in the setting of long-term lead exposure and is often associated with hypertension and gout. Diagnosis of chronic lead nephropathy is more difficult since the laboratory abnormalities seen with acute lead intoxication are not present with chronic lead exposure. The typical clinical picture and the exclusion of other causes of renal disease allow the diagnosis of chronic lead nephropathy to be made. Evaluation of lead stores by either the calcium disodium edetate (EDTA) mobilization test or K-x-ray fluorescence are helpful in clinching the diagnosis. Treatment with EDTA lead mobilization is effective for acute lead poisoning while avoidance of further lead exposure prevents recurrence of lead intoxication. Treatment of chronic lead nephropathy with EDTA lead mobilization is useful if renal failure is modest; however, EDTA mobilization is of no benefit in patients with more severe renal insufficiency.

Hyperkalemia is a serious electrolyte disorder which appears to develop more commonly in the aged patient. The elderly may be predisposed to hyperkalemia as a result of underlying abnormalities in potassium homeostasis. These include inapparent renal insufficiency, tubulointerstitial disease in the kidney, disturbed aldosterone production, and abnormal salt and water balance. Several commonly prescribed medications may further disrupt potassium balance and promote the development of hyperkalemia in these patients. Trimethoprim-sulfamethoxazole, a commonly used antimicrobial agent, has recently been noted to cause hyperkalemia in the elderly, even with standard dosage. The elderly should be considered at high risk to develop hyperkalemia, especially when they are using certain medications. Potassium concentration should be monitored closely when these patients are hospitalized and/or treated with potassium-altering medications.

Transesophageal echocardiography (TEE) is a useful clinical tool for the evaluation of a variety of cardiovascular lesions. In particular, TEE has been demonstrated to be a better diagnostic modality in the visualization of mechanical prosthetic heart valves than transthoracic echo-cardiography (TTE). Furthermore, TEE is noted to be particularly useful to evaluate the atrial surface of mitral prostheses, the usual location of thrombi or vegetations. We herein describe a patient with a dysfunctional St. Jude's mitral prosthesis resulting from an organized thrombus who underwent both TTE and TEE without visualization of the thrombus.

Melanoma is a cutaneous malignancy with an incidence that is rising. Surgery is curative if performed prior to metastasis. Liver metastasis is common and is often associated with an elevation in lactic dehydrogenase. A rise in transaminases is unusual; typically it is low in these patients. We describe a case of metastatic melanoma which presented as severe hepatocellular disease.