Relation between myocardial infarction, depression, hostility, and death.

OBJECTIVE: To examine the independent impact of major depression and hostility on mortality rate at 6 months and 12 months after discharge from the hospital in patients with a myocardial infarction. METHOD: Three hundred thirty-one patients were prospectively evaluated for depression with a modified version of the National Institute of Mental Health Diagnostic Interview Schedule for major depressive episode. The Cook Medley Hostility Scale data were analyzed by chi(2) procedures for nominal and categoric data, and Student t test was used for continuous data types. RESULTS: Depression was a significant predictor of death at 12 months (P =. 04) but not at 6 months (P =.08). Hostility was not found to be a predictor of death at 6 months or 12 months. CONCLUSIONS: Major depression in patients hospitalized after myocardial infarction is a significant univariable predictor of death at 12 months, although it was not a statistically significant predictor after adjusting for other variables. Hostility is not a predictor of death. Prospective studies are needed to determine the impact of aggressive treatment of depression on post-myocardial infarction survival.

Urinary doubly refractile lipid bodies in nonglomerular renal diseases.

Urinary doubly refractile lipid bodies (DRLB) are a characteristic finding in patients with glomerular renal diseases causing heavy proteinuria. DRLB are felt to be an uncommon finding in glomerular diseases without heavy proteinuria, and a rare finding in nonglomerular renal diseases. In order to determine whether DRLB are found in nonglomerular renal diseases, we reviewed the medical records of all patients who had urinalyses performed in our laboratory from February 1975 to June 1983. Three hundred sixty one patients demonstrated less than or equal to +2 proteinuria, and at least two DRLB. Of these, 290 were identified as having a single renal diagnosis. One hundred forty eight patients (51%) had a variety of acute and chronic glomerular diseases, and 125 patients (43.2%) had nonglomerular renal diseases, including acute tubular necrosis (ATN), prerenal azotemia, chronic interstitial nephritis, polycystic kidney disease, acute interstitial nephritis, renal neoplasia, and acute myeloma kidney. Ten patients had transient proteinuria associated with acute illness, and seven patients had no renal disease at all. Only two patients with nonglomerular renal disease had more than five DRLB per 20 high power microscopic fields. The frequency of DRLB in patients with nonglomerular renal diseases was: chronic interstitial nephritis, 26%; polycystic kidney disease, 38%; prerenal azotemia, 20%; ATN, 15%; and acute interstitial nephritis, 33%. These data suggest that at lower levels of proteinuria, DRLB are found frequently in nonglomerular renal diseases, and that DRLB do not differentiate glomerular from nonglomerular renal diseases unless more than five DRLB are found on urinary sediment examination.

Renal angiomyolipoma with arteriovenous shunting.

We describe a patient with arteriovenous shunting during renal arteriography who at operation was found to have an angiomyolipoma rather than renal cell carcinoma or an arteriovenous malformation. Renal angiomyolipoma should be added to the list of causes of gross hematuria with angiographically demonstrable arteriovenous shunting.

Syndrome of inappropriate antidiuresis in Waldenström's macroglobulinemia.

Hyponatremia due to the syndrome of inappropriate antidiuresis rather than due to isotonic hyponatremia from hyperproteinemia developed in a patient with Waldenström's macroglobulinemia. The patient was unable to excrete a water load normally despite suppression of antidiuretic hormone to normal levels. The temporal relationship between control of the tumor and resolution of the hyponatremia suggests that the tumor either produced a substance that enhanced the hydro-osmotic effect of endogenous antidiuretic hormone or produced an antidiuretic substance immunologically different from antidiuretic hormone. The syndrome of inappropriate antidiuresis should be suspected in hyponatremic patients with Waldenström's macroglobulinemia.

Impaired potassium and magnesium homeostasis in acute tubulo-interstitial nephritis.

Although acute tubulo-interstitial nephritis is increasingly recognized as a cause of acute renal failure, little is known about renal tubular function in this disease. We report on two patients with acute tubulo-interstitial nephritis who demonstrated abnormalities in proximal and distal tubular function. The first patient developed hyperkalemia presumably from a potassium secretory defect in the distal nephron. The second patient developed an incomplete Fanconi's syndrome with glycosuria and aminoaciduria and two heretofore unreported complications of acute interstitial nephritis: hypokalemia and hypomagnesemia secondary to urinary losses of these cations. Careful monitoring of renal tubular function is indicated in patients with acute tubulo-interstitial nephritis.

Amelioration of hemodialysis-induced fall in PaO2 with exercise.

The hypoxemia of acetate hemodialysis may result from a decrease in alveolar ventilation (VA) related to a reduction in pulmonary carbon dioxide excretion (VCO2). To test this theory, ventilation was increased by exercise during dialysis on 6 patients and the effect on arterial oxygen tension (PaO2) measured. With hemodialysis the PaO2 fell from 102 to 92 mm Hg and with exercise rose to 102 mm Hg. These changes in PaO2 paralleled changes in VA and VCO2 induced by acetate dialysis and then exercise. The correlation coefficient between VA and VCO2 was 0.997. This close correlation suggests that CO2 load may be the main controlling factor for ventilation under these conditions. We conclude that the fall in PaO2 that occurs with acetate hemodialysis is due to decreased ventilation secondary to decreased VCO2 and that exercise can ameliorate the fall in PaO2 by increasing ventilation.

Failure of chelation therapy in lead nephropathy.

A patient with lead nephropathy and gout was treated with three months of edetic acid chelation. The therapy resulted in normalization of a previously abnormal result of edetic acid lead mobilization test. Nevertheless, progressive renal insufficiency occurred. At autopsy, an increased bone lead content was documented, suggesting that the edetic acid lead mobilization test may underestimate total body lead stores and that chelation therapy may not be effective in reversing advanced lead nephropathy. Alternatively, a longer period of therapy may be necessary to remove lead stores. More studies are needed to determine the relationship between the results of the edetic acid test and bone lead stores. Methods other than the edetic acid lead mobilization test should be considered to monitor the adequacy of treatment in lead nephropathy.

Synergistic effect of acute renal failure and respiratory failure in the surgical intensive care unit.

A retrospective evaluation of the effect of renal and respiratory failure on mortality in our surgical intensive care unit was undertaken. The coexistence of combined renal and respiratory failure had a synergistic adverse effect on survival. Combined pulmonary and kidney failure appeared to develop simultaneously. A subset of patients with severe prerenal azotemia but without uremia had the highest mortality. These results are not consistent with the simple combination of single systems failure but rather suggest that renal and respiratory failure are makers of a generalized underlying defect.

Dependence of saline-induced natriuresis upon exposure of the kidney to the physical effects of extracellular fluid volume expansion.

In many previous studies, the natriuresis induced by saline loading has been demonstrated to persist even though glomerular filtration rate (GFR) has been decreased to below pre-expansion levels by a reduction in renal artery pressure. In such studies, however, the kidney has been exposed to the effects of volume expansion for varying periods of time before renal artery pressure was controlled. The present experiments were designed to evaluate whether this period of exposure induces critical changes in intrarenal factors that are responsible for the natriuresis.Experiments were carried out in rats, in which renal artery pressure was decreased to 70 mm Hg either at the onset of saline loading (immediate clamping experiments) or after 45 min of saline loading had elapsed (delayed clamping experiments). In the delayed clamping experiments, consonant with previous studies, mean sodium excretion, 3.2 mueq/min, remained markedly increased above control, despite a reduction in GFR to 91% of the hydropenic control value. In contrast, when renal artery pressure was comparably reduced at the onset of saline loading mean sodium excretion was only trivially increased, 0.4 mueq/min, although GFR increased to 140% of the hydropenic control value. These results exclude an important role for either a circulating hormone or a reduction in plasma oncotic pressure in the natriuretic response to saline loading, and indicate that intrarenal factors are the critical determinants of the natriuresis. We have used the difference in response to saline loading in the immediate and delayed clamping experiments to evaluate the role of two intrarenal factors, interstitial hydrostatic pressure and renal plasma flow. Interstitial pressure changes were estimated from changes in tubular pressure and diameter by using the in situ compliance characteristics of the tubules. In a group of rats saline loaded without aortic clamping, interstitial pressure increased by 4-5 mm Hg and renal plasma flow increased by 2.5 ml/min. During the period of reduced renal artery pressure, however, neither interstitial pressure nor renal plasma flow was detectably increased above control in either the immediate or the delayed clamping experiments. The only noteworthy difference between the experiments in which a natriuresis occurred (unclamped and delayed clamping studies) and the experiments in which no natriuresis occurred is that in the former group the kidney was at least transiently exposed both to an increase in renal plasma flow and interstitial pressure. These findings indicate, first, that extracellular fluid volume expansion can induce a natriuresis only if the kidney has been exposed to at least a transient increase in either interstitial hydrostatic pressure or renal plasma flow (or both); and, second, that a sustained increase in interstitial pressure and renal plasma flow is not required for the natriuresis to persist.