Severe hyperphosphatemia induced by a phosphate-containing oral laxative.

OBJECTIVE: To describe a case of severe hyperphosphatemia following unintentional overdosage with an oral phosphate laxative, and raise attention to the risk of using such medications in the elderly. CASE SUMMARY: An 84-year-old white woman was admitted with confusion 8 hours after inadvertently ingesting 12 fluid ounces of Fleet Phospho-Soda (instead of the prescribed 1 1/2 fluid ounces) prior to a colonoscopy. Her serum phosphate and ionized calcium concentrations were 10.3 mmol/L and 0.56 mmol/L, respectively. She was treated conservatively with oral phosphate binders and made an uneventful recovery. DISCUSSION: Several previous reports have described hyperphosphatemia in association with phosphate laxatives, especially in patients with renal or colonic disease. Our case again presents two important issues in the use of phosphate laxatives by the elderly: (1) the frequently overlooked underlying renal insufficiency in which, despite "normal" serum creatinine values, renal phosphate handling may be impaired; and (2) the potential for drug misuse and poor compliance in the elderly. CONCLUSIONS: Caution should be taken with the use of phosphate laxatives in the elderly in the face of potentially serious metabolic abnormalities that may be generated.

Low plasma renin activity in normotensive patients with diabetes mellitus: relationship to neuropathy.

To determine the effect of diabetes mellitus on the renin-aldosterone system, independent of age, nephropathy, or hypertension, 16 normotensive diabetics with long-term disease (mean duration, 15 years) and no (14) or minimal (2) proteinuria, were compared to nine age-matched, normotensive controls. Plasma renin activity (PRA) measured supine and after 4 hours of quiet ambulation, both on an ad libitum diet and on Day 4 of a 10 mEq low sodium diet, was always lower in the diabetics (31%-56% of control values). After the combined stimulus of sodium depletion and ambulation, PRA was 2.2 +/- 0.4 in the diabetics compared to 3.4 +/- 0.2 ng/ml/hr in controls (p less than 0.025). On the low sodium diet, PRA and the postural response of PRA correlated directly with the degree of autonomic dysfunction as quantitated by the velocity of esophageal peristalsis (r = 0.60, p less than 0.05; r = 0.75, p less than 0.005 respectively), suggesting that autonomic neuropathy was an important factor contributing to low PRA in these patients. No other parameters correlated with PRA. Plasma renin substrate (PRS) tended to be lower in diabetics (1053 +/- 95 vs 1358 +/- 132 ng AI/ml; p less than 0.07) but not sufficiently so to account for the substantial difference in PRA. Furthermore, PRS did not correlate with PRA. Fasting blood sugar, while higher in diabetics (209 vs 96 mg/dl), and creatinine clearance, which was lower (112 +/- 13 vs 78 +/- 4 ml/min; p less than 0.01), also did not correlate with PRA. Other factors, including serum creatinine, serum potassium, urinary aldosterone, blood pressure, and body weight, and the responses of these parameters to sodium depletion, were similar in diabetics and controls. These data implicate visceral neuropathy as a major factor in the hyporeninemia of these diabetics.

Skeletal responsiveness in pseudohypoparathyroidism. A spectrum of clinical disease.

Three cases of pseudohypoparathyroidism with roentgenographic evidence of hyperparathyroid bone disease are described. Renal resistance to exogenous parathyroid hormone (PTH), the hallmark of pseudohypoparathyroidism, was documented by markedly blunted or absent urinary phosphate and cyclic AMP responses to parathyroid extract. At the time of diagnosis all patients were hypocalcemic and hyperphosphatemic with elevated serum alkaline phosphatase levels and subperiosteal resorption noted on skeletal films. Bone biopsy in one patient revealed a histologic appearance consistent with hyperparathyroidism. Serum PTH levels, measured in two patients while they were hypocalcemic, were elevated. None of the patients had short stature, brachydactyly, subcutaneous calcification or mental deficiency. These cases are compared to the 15 well-documented cases previously reported. The presently available information on pseudohypoparathyroidism indicates a variable skeletal response to PTH mediated by several factors extrinsic to bone and suggests that pseudohypoparathyroidism with hyperparathyroid bone disease is one extreme of a clinical spectrum of skeletal responsiveness to PTH. This disorder is part of an expanding clinical picture which makes pseudohypoparathyroidism a diagnostic consideration in any patient with unexplained hypocalcemia, hyperphosphatemia, elevated alkaline phosphatase levels or metabolic bone disease.

Age and the renin-aldosterone system.

Age effect on plasma renin activity (PRA) and PRA classification was studied in young and older normotensive volunteers. Ambulatory PRA was lower in the older age group than in the younger with both on an unrestricted diet and a low-sodium diet. Renal function, aldosterone excretion, and plasma renin substrate were comparable in both groups. Age had a substantial effect on PRA classification. When the young normotensives were controls, 32% (6/19) older normotensives had abnormally low PRA, or "low renin normotension." Similarly, 18% (2/11) of young patients with essential hypertension but 80% (12/15) of older hypertensives had low PRA. When the older volunteers were controls, however, the incidence of low renin hypertension (LRH) decreased to 53% in the older patients. The use of predominantly young controls for defining normal limits of PRA may result in an overestimate of the incidence of LRH and may contribute to the heterogeneity of LRH.