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Contrast nephropathy is an adverse alteration in renal function induced by intravascular contrast media. Most cases involve transient asymptomatic episodes; yet a significant number involve oliguria and/or permanent renal damage. The incidence of contrast nephropathy in the general hospitalized population is about 5%, and is associated with preexisting renal insufficiency and diabetes mellitus. The incidence in patients with normal renal function is significantly lower - 0.6% following IVP and 2% following angiography. Angiography carries risks inherent to the technical problems of the procedure itself. Preexisting renal insufficiency is the most significant predisposing condition of contrast nephrotoxicity. As many as two-thirds of patients with chronic renal failure may experience an acute deterioration in renal function following exposure. Most of these episodes are transient and benign. Diabetic patients with preexisting renal insufficiency are at an even greater risk; about 75% of such patients will experience renal complications. The risk is even higher in JODM patients with severe renal disease; there is an over 90% incidence of nephrotoxicity with as many as half sustaining permanent renal damage. Adequate hydration does not appear to reduce the incidence of contrast nephropathy in susceptible patients, but it may reduce the likelihood of oliguria and permanent damage. In multiple myeloma the risk of contrast-induced renal failure is low, and probably involves a different pathogenesis than seen in other cases of contrast nephropathy. The incidence in myeloma patients is probably increased in the presence of dehydration and renal insufficiency. Peripheral vascular disease, hypertension, old age and large and repeated doses of contrast may increase the risk in susceptible patients. Prevention of contrast nephropathy must start with identification of patients at risk. In patients with preexisting renal insufficiency, and especially diabetic patients with preexisting renal insufficiency, the anticipated benefit should outweigh the potential risk of exposure to contrast media.
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PMID:Contrast nephropathy. 675 74

The clinical and diagnostic features of renal papillary necrosis (RPN) of 27 patients were studied. Diabetes mellitus was the most frequent (56%) condition associated with RPN. Analgesic abuse, sickle hemoglobinopathy and urinary tract obstruction were present in 4 patients each; in 6 of these 12 patients these conditions were present as a coexistent disease with diabetes mellitus. There was evidence of an acute or chronic infection of the urinary tract in 18 patients, as a coexistent condition with another underlying disease that itself can cause RPN in 14 patients and as the only cause of RPN in another 4. Thus, the presence of more than one diagnostic condition which might be implicated in the causation of RPN was present in 15 patients or 55% of the cases in this series. When infection was excluded, six patients or 22% of the cases had two coexisting diseases, each of which has been implicated as a cause of RPN. This observation underlines the multifactorial nature of this entity and might explain why RPN is not encountered more frequently in each of the various primary diseases with which it has been associated. The average age of the patients at the time of diagnosis was 53 years for women and 56 years for men. Only six of the patients were younger than 40 years, and three of these had sickle hemoglobinopathy. The diagnosis of RPN was based on x-ray findings in eight patients, on the histologic examination of papillary tissue in urine in one, and on autopsy findings in the rest. Papillary necrosis was bilateral in three-fourths of the cases. The clinical picture varied. Most of the patients (67%) presented with chills and fever. Flank pain and dysuria were present in 11 patients (41%). As a rule oliguria was rare and progressive uremia was uncommon. In cases diagnosed at post-mortem, the patients had succumbed to infection or to a primary severe extrarenal disorder with the possibility of RPN having been entertained clinically in only half these cases prior to autopsy.
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PMID:Renal papillary necrosis: an update. 703 74

Risk factors, clinical courses, and urinary indices were examined in 12 consecutive patients with contrast media-induced acute renal failure. A high prevalence of preexisting renal disease, diabetes, vascular disease, and compromised cardiac output was observed. All patients had transient oliguria one to four days in duration, and all patients had return of renal function to their baseline values within five to ten days. Consistently low urinary sodium concentration and fractional excretion of sodium (FENa) were seen during the oliguric phase of the acute renal failure. Fractional excretion of sodium of less than 1% persisted for up to five days despite unequivocal renal function deterioration. The findings raise the possibility that acute renal failure secondary to contrast media may be mediated either by decreases in renal perfusion or by acute tubular obstruction.
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PMID:Low fractional excretion of sodium with contrast media-induced acute renal failure. 736 85

The renal venous thrombosis is mostly produced by severe dehydration. The following, however, are also predisposing factors: infections, birth traumata, paranephritic processes, lack of oxygen, diabetes of the mother and cyanotic heart defects. The diagnosis is correctly made by means of the palpable flank tumor, the macrohematuria, together with the urogram and sonography. The most urgent therapeutic measure is the balancing of the water and electrolyte deficit to eliminate the dehydration, i.e. the existing oliguria or anuria. The therapy is primarily always conservative. In the event of a consumption coagulopathy, a therapeutical attempt can be undertaken with heparin but if this is unsuccessful, an immediate nephrectomy must be performed. A further nephrectomy will be necessary if hypertony persistent infection and renal atrophy occur. Two infants with renal venous thrombosis were used for this study on the causes and diagnosis of, and the therapy for the illness.
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PMID:[Renal venous thrombosis in the newborn (author's transl)]. 746 39

On the basis of examination of 634 patients with acute surgical endotoxemia in patients with diabetes mellitus the following features have been revealed: hypertonic dehydration has dominant as well as hyperkalemia, marked hyperazotemia. Oliguria was detected only in 18.8% of patients. Plasmic osmolarity was 296-348 mosm/l, predominantly for account of hyperazotemia and hyperglycemia. 86.97% of patients showed ketoacidosis. The scheme of intensive therapy of surgical endotoxemia in patients with decompensative diabetes mellitus with programme applications for paternal computers is suggested.
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PMID:[The possibilities for correcting hydro ion metabolism in acute surgical pathology in diabetics]. 762 26

An 80-year-old woman with diabetes mellitus was treated with gliclazide. Prior to the gliclazide administration, her urinary excretion of albumin, serum urea nitrogen and serum creatinine were normal. After the medication, oliguria, edema and azotemia developed. On the twenty-fourth day when the edema was severe and generalized, gliclazide administration was terminated. On the following day urinary volume increased suddenly (5,740 ml/day). Polyuria persisted for five days. Edema improved and urea nitrogen and creatinine were normalized thereafter. Though the mechanism is not known, the clinical course suggests that gliclazide is the principal causative factor in the water retention and azotemia in this patient.
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PMID:Possible gliclazide-induced water retention with azotemia. 806 94

We report a patient with rhabdomyolysis secondary to hyperosmolar nonketotic diabetic coma (HNKC), who progressed to acute renal failure. A 43-year-old male with diabetes mellitus for three years was admitted to our hospital because of loss of consciousness. The laboratory findings at admission were as follows: serum glucose 1792 mg/dl, serum Na 129 mEq/1, BUN 71 mg/d1, serum creatinine 3.3 mg/d1, CPK 715 IU/1, plasma osmolality 370 mOsm/1, and negative urine ketone bodies. A diagnosis of HNKC was made. On the 2nd day, he had oliguria and the serum creatinine increased despite adequate treatment of HNKC by the administration of intravenous fluid and insulin. On the 4th day, CPK reached 47,300 IU/1, and serum myoglobin was also increased, indicating rhabdomyolysis. His renal function improved gradually and was almost normalized on the 20th day. Renal biopsy on the 23rd day showed myoglobin at the distal renal tubules, which appeared to be involved in the pathogenesis of renal failure by rhabdomyolysis. However, we found little abnormality association with diabetic nephropathy in the renal tissue. Since HNKC is known to induce acute renal failure rarely without diabetic nephropathy, these findings suggested that the acute renal failure was caused mainly by the rhabdomyolysis. Acute renal failure induced by rhabdomyolysis in patients with HNKC is rare, but fatal. The present study showed that the measurement of serum CPK and urine myoglobin was helpful for early diagnosis. Only 12 cases have been reported to have developed renal failure due to rhabdomyolysis among patients with HNKC. To our knowledge, we demonstrated for the first time that myoglobin at the distal renal tubules after renal function was normalized.
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PMID:[Rhabdomyolysis related-acute renal failure in a patient with hyperosmolar nonketotic diabetic coma (HNKC): demonstration of myoglobin casts after normalization of renal function]. 882 59

Fluid retention develops relatively early in the renal insufficiency of patients with diabetic nephropathy. The objective of this study was to clarify the effect of postural change on urine volume and urinary sodium excretion in diabetic nephropathy. Subjects consisted of 16 patients with non-insulin-dependent diabetes mellitus (five with diabetic nephrotic syndrome [DNS], five with nonnephrotic overt diabetic nephropathy [NNODN], and six without overt diabetic nephropathy [ODN]) and 11 patients with nondiabetic renal diseases (five with nondiabetic nephrotic syndrome [NDNS] and six without nephrotic syndrome). Patients were studied during 60 minutes of recumbency, followed by 60 minutes of standing. Mean blood pressure decreased in the standing posture only in patients with DNS and nondiabetic renal diseases. Urine volume decreased in the standing posture in the three groups of diabetic patients. Urine volume showed no changes in the standing posture in nondiabetic patients with and without nephrotic syndrome. The decreases in mean blood pressure and urine volume and the percentage decrease in creatinine clearance were significantly larger in patients with DNS than in those with NDNS and NNODN. The increase in free water clearance was significantly smaller in patients with DNS than in those with NDNS and NNODN. Urinary sodium excretion decreased in the standing posture in diabetic and nondiabetic patients, while no differences in the magnitude of changes were noted among patients with NDNS, NNODN, and DNS. It is concluded that the standing posture causes a greater decrease in urine volume due to orthostatic hypotension in patients with DNS compared with those with NDNS and NNODN, and that the presence of orthostatic hypotension in patients with DNS is likely responsible for the greater fluid retention of this group compared with other nephrotic patients with similar degrees of hypoalbuminemia.
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PMID:Effect of postural change on urine volume and urinary sodium excretion in diabetic nephropathy. 942 50

At the beginning of this century, the diagnosis of various renal diseases was made with relative accuracy although neither plasma markers of glomerular filtration nor renal biopsy nor imaging were available. Renal edema was identified by high albuminuria, hyalin cylinders, high urine density and oliguria. Renal hematuria was detected by cylinders of erythrocytes. Hallmarks of chronic renal insufficiency, recognized at autopsy by atrophic kidneys, were hyposthenuria, polyuria and slight albuminuria without edema associated with arterial hypertension, anemia, retinopathy and left ventricular hypertrophy. The detection of increased plasma volume in experimental toxic nephritis by St. Moscati proposed the underlying mechanism of arterial hypertension. Experimental and clinical research in the preinsulin era indicated the central role of the kidney in the functional alterations induced by diabetes. Indeed, glucosuria was known to appear only when glycemia was relatively high. The kidney appeared enlarged and hyperemic, i.e. the so-called glomerular hyperfiltration. Glucosuria was directly correlated with diuresis but it markedly decreased in renal insufficiency. In diabetes complicated by nephropathy, tolerance to carbohydrates improved. Correction of glucosuria by dietary treatment was followed by a prompt rise in body weight, due to retention that counterbalanced the previous losses. Diabetic ketoacidosis, determined by the measurement of urinary ketonic body excretion, was treated with sodium bicarbonate (30-50 g/day in severe acidosis) up to achieving an alkaline urine pH. It was known that high doses of sodium bicarbonate might induce edema which gradually disappeared with a reduction in the alkaline administration. Clinical significance of sodium balance was, in fact, recognized: the external NaCl balance between alimentary ingestion and urinary excretion was neutral in normal conditions and became positive at high body temperature or negative during reabsorption of exudates.
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PMID:Diagnosis of renal disease at the beginning of the 20th century. 1021 38

The steroid-sparing effect and the use of concomitant medication during the treatment of liver transplant patients with the novel immunosuppressant FK 506 were evaluated within the European multicentre, randomized, parallel-group study in liver transplantation. Patients undergoing primary liver transplantation were randomized to treatment with FK 506 (n = 267) or with a cyclosporin-based immunosuppressive regimen (n = 273). The total cumulative steroid usage was significantly reduced in the FK 506 treatment group, which is likely to have resulted from the lower incidence of acute rejection in these patients. The number of patients receiving antidiabetic, diuretic and antihypertensive therapy did not differ between the two treatment groups, even though the incidence of diabetes mellitus and oliguria was significantly higher in the FK 506 group. It can, therefore, be assumed that in a number of such cases the severity of these events was very mild necessitating no specific therapy.
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PMID:Corticosteroids and concomitant medication in the European multicentre study of FK 506 and cyclosporin in primary liver transplantation. 1127 38


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