ABSTRACT
Polyuria is an important symptom or sign because of its potential severity, diverse causes, and interesting pathophysiology. Whereas polyuria induced by water diuresis is reasonably well understood and easily recognized by clinicians, that produced by solute diuresis is more likely to cause confusion. In this article, we focus on solute diuresis as a cause of polyuria, review the classification and pathophysiology of polyuria, and describe the clinical and laboratory studies useful for the evaluation of the polyuric patient. A stepwise, logical approach is provided (1) to determine whether a patient has a water diuresis, a solute diuresis, or both (concurrently), and (2) if a solute diuresis is present, to determine if it is caused by electrolytes (eg, sodium chloride sodium bicarbonate), by nonelectrolytes (eg, glucose, urea), or by both. How to assess these possibilities and to determine the specific cause of the diuresis is discussed in detail. Three representative case examples are provided. Selected causes of a solute diuresis also are reviewed.
Subject(s)
Diuresis , Polyuria/etiology , Polyuria/physiopathology , Adult , Algorithms , Decision Making , Diagnosis, Differential , Female , Humans , Male , Middle AgedABSTRACT
Although the exact incidence of drug-induced nephrotoxicity is not known, it is important for clinicians to be aware of the risks in certain patients and to know which drugs are the most commonly implicated. The latter include radiocontrast agents, aminoglycosides, nonsteroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors. Other medications also have nephrotoxic potential when they are prescribed in specific patient populations. Renal injury may be transient and mild in many cases, but recognition of the patient at high risk and application of preventive measures are essential to avoid a severe and protracted course.
Subject(s)
Kidney Diseases/chemically induced , Aminoglycosides/adverse effects , Angiotensin-Converting Enzyme Inhibitors/adverse effects , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Contrast Media/adverse effects , Humans , Kidney Diseases/diagnosis , Kidney Diseases/physiopathology , Kidney Diseases/prevention & control , Male , Middle Aged , Risk FactorsABSTRACT
A patient with a markedly elevated serum phosphorus level (23.9 mg/dL) is described, followed by a brief review of severe hyperphosphatemia. Elevated serum phosphorus levels may be artifactual or true. True hyperphosphatemia is usefully subdivided according to (a) whether phosphorus is added to the extracellular fluid from a variety of exogenous or endogenous sources, or (b) whether the urinary excretion of phosphorus is reduced from either decreased glomerular filtration or increased tubular reabsorption. Severe hyperphosphatemia, defined herein as levels of 14 mg/dL or higher, is almost invariably multifactorial--usually resulting from addition of phosphorus to the extracellular fluid together with decreased phosphorus excretion. The hyperphosphatemia of the patient described herein appeared to result from a combination of dietary phosphorus supplementation, acute renal failure, acute pancreatitis, and ischemic bowel disease, complicated by lactic acidosis.
