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PubMed1979

Single dose whole pelvis megavoltage irradiation for palliative control of hematuria or ureteral obstruction.

Of 7 patients with bladder carcinoma whose medical condition or disease status prevented an operation 5 had intractable vesical hemorrhage and 2 had progressive azotemia caused by ureteral obstruction. These patients were treated with pelvic irradiation of 1,000 rad single doses. Four patients received 3 doses 3 to 4 weeks apart and 1 patient received 2 doses at a 4-week interval. Prompt cessation of bleeding occurred in all patients and renal function improved in the 2 patients with ureteral obstruction.

Aged↗
PubMed1979

Association of crossed fused renal ectopia and multicystic kidney.

A male newborn presented with mild azotemia, an abdominal mass and non-visualized right kidney on excretory urography. Evaluation, including ultrasound and surgical exploration, revealed the simultaneous occurence of crossed fused renal ectopia and multicystic kidney.

Humans↗
PubMed1977

Augmentation enterocystoplasty: a critical review.

Augmentation cystoplasty appears to offer a successful long-term solution for patients with small contracted bladders of almost any etiology. If proper indications are observed the procedure is well tolerated. With refined urodynamic diagnostic techniques our over-all failure rate of 35 per cent can be expected to decrease. Contraindications of the procedure include azotemia (creatinine clearance less than 40 cc per minute), vesical malignancy, neurogenic bladder with spastic pelvic floor (that cannot be modified) and young boys (mucus problems). In addition, patients with a strong psychiatric history should be approached with caution. The non-functional contracted bladder in which the cause of prior diversion is unclear or was performed because of an apparent outflow obstruction that spontaneously has been corrected by rest during the period of supravesical diversion also should be approached with care.

Adolescent↗
PubMed1977

Perinatal asphyxia and renal failure in neonatal patients.

Herein we discuss oliguria and azotemia in neonatal patients associated with perinatal complications, including difficult labor and delivery, and respiratory asphyxia. Renal failure in these patients is accompanied by proteinuria, microscopic hematuria and red blood cell casts, and it generally resolves in 7 to 10 days. Umbilical aortography can be helpful in determining the presence of normal kidneys in these patients.

Asphyxia Neonatorum↗
PubMed1977

Severe metabolic acidosis as a complication of intravenous tetracycline therapy.

Tetracycline generally is believed to be a safe drug with relatively minor side effects. Serious irreversible renal damage and metabolic acidosis can occur in patients with azotemia. While the exact mechanism is unknown, the commonly reported nephrotoxic and metabolic effects of tetracycline are reviewed and an illustrative case is presented.

Acidosis↗
PubMed1977

Surgical treatment of the massively dilated ureter in children. Part I. management by cutaneous ureterostomy.

One of the major therapeutic challenges facing the pediatric urologist is the massively dilated ureter. When conservative measures, such as relief of obstruction or treatment of infection, have failed or are likely to fail, surgical treatment must be directed at the massive dilatation itself. These circumstances were encountered in 366 massively dilated ureters in 244 children during a 10-year period. Loop and/or terminal cutaneous ureterostomy was used to manage 125 of these ureters in 74 children. Indications for temporary non-intubated proximal urinary diversion included uncontrolled infection, sepsis, azotemia, significant ureteral redundancy and tortuosity, and questionable over-all renal function. Advantages of loop ureterostomy included more proximal drainage and less stomal problems but terminal ureterostomy required a significantly lesser number of surgical procedures in reconstructing the urinary tract. Temporary splinting of the ureter in dry ureteral reimplantations has diminished markedly the incidence of ureterovesical complications. No instances of permanent vesical contracture were noted after long periods of defunctionalization. After initial reconstruction of 47 cutaneous ureterostomies good results by all parameters were obtained in 68 per cent. Additional surgical procedures in selected initial failures have resulted in a final success rate of 85 per cent.

Dermatologic Surgical Procedures↗
PubMed1976

Diagnosis and treatment of a urinary leak after ureteroileal conduit for diversion.

Of 1,120 cases of ileal loop urinary diversion reviewed from our hospital 21 postoperative loop leaks were noted (1.87 per cent). Definite indications for diagnostic studies of urinary extravasation include persistent postoperative azotemia, sepsis and/or urinary leakage via the drains. In this series 2 types of loop leaks were noted--an early postoperative leak within the first 24 hours and a leakage 6 to 12 days postoperatively. More aggressive management of postoperatively urinary extravasation is urged, especially in patients who had been irradiated and suffered leakage later on in the postoperative course.

Adolescent↗
PubMed1976

Unilateral renal agenesis presenting as anuria.

The most common cause of sudden and total cessation of urine output is obstructive uropathy, usually at the bladder outlet. Bilateral ureteral obstruction is a much less common cause of anuria. In additioh, unilateral obstruction in the presence of a solitary kidney must be considered in the differential diagnosis. Primary renal parenchymal disorders and pre-renal azotemia occasionally may be anuric but more commonly are oliguric. A case of unilateral renal agenesis presenting as anuria and obstruction of the solitary kidney is described.

Anuria↗
PubMed1976

Acute interstitial nephritis.

Acute allergic interstitial nephritis is manifested clinically by rash, fever, eosinophilia, hematuria, oliguria and azotemia. Histologically a monocytic inflammatory process in the renal interstitium is seen. The clinical course of a patient after excessive sodium cephalothin administration suggested allergic interstitial nephritis and implicates this drug as an etiologic agent.

Acute Disease↗
PubMed1992

Balance studies and polymeric glucose solution to optimize therapy after massive intestinal resection.

The aim of this study was to determine whether fluid homeostasis could be maintained by using a hypo-osmolar (200 to 221 mosmol/kg), relatively low-sodium (50 to 52 mmol/liter) solution that contained a glucose polymer in a 54-year-old patient with high ileostomy output attributed to short-gut syndrome and resultant prerenal azotemia. Sequential balance studies were performed to assess stool and urinary output, stool fat, and urinary electrolytes initially during intravenous rehydration and subsequently during administration of the necessary fluids and nutrients exclusively by oral supplementation. The additional effects of high-fat and low-fat diet, loperamide hydrochloride, and octreotide acetate were evaluated. When the patient sipped a hypo-osmolar oral rehydration solution while she was awake during the day and received a high dose of loperamide and a 40-g fat, disaccharide-free diet, salt and water homeostasis was maintained. The addition of octreotide did not substantially enhance fluid balance; rather, it increased fecal fat and fluid losses from the small bowel. Thus, hypo-osmolar polymeric glucose solutions maintain fluid homeostasis in patients with the short-gut syndrome. In such patients, simple balance studies are useful for assessing the absorptive capacity of the residual intestine, for developing an optimal individualized treatment, and for eliminating the need for costly, long-term home parenteral nutrition.

Crohn Disease↗
PubMed1990

Acute uric acid nephropathy.

Uric acid, as the end-product of purine metabolism in humans, presents a clinical problem because of its relative insolubility, particularly in the acid environment of the distal nephron of the kidney. As a result, states of enhanced purine catabolism increase the urate load on the kidney, leading to intrarenal precipitation. Major causes of increased purine metabolism are malignancies with rapid cell turnover, such as leukemias and lymphomas, and the added acceleration of cell lysis that occurs with chemotherapy and radiation. Serum urate levels rise rapidly, and acute renal failure occurs as a consequence of tubular deposition of urate and uric acid. The keys to the diagnosis of acute uric acid nephropathy are the appropriate clinical setting of increased cell lysis, oliguria, marked hyperuricemia, and hyperuricosuria. A urinary uric acid-to-creatinine ratio greater than 1 helps to distinguish acute uric acid nephropathy from other catabolic forms of acute renal failure in which serum urate is elevated. Preventive treatment involves pharmacologic xanthine oxidase inhibition with allopurinol and alkaline diuresis. Occasionally, acute renal failure occurs despite allopurinol because of the tubular precipitation of the precursor metabolites, such as xanthine, which accumulate with xanthine oxidase inhibition. Dialysis therapy may be required both to correct azotemia and to reduce the body burden of urate. Hemodialysis is preferred because it can achieve greater clearance than other dialysis modes.

Acute Disease↗
PubMed1990

Drug-induced nephropathies.

Drug-induced renal disease is a common problem. Drugs cause several renal syndromes, such as prerenal azotemia, fluid and electrolyte abnormalities, acute tubular necrosis, acute interstitial nephritis, and chronic interstitial nephritis. Acute renal failure due to acute tubular necrosis is the most common syndrome and is most frequently caused by aminoglycoside antibiotics, radiographic contrast agents, and amphotericin B. Avoidance of these drugs in volume-depleted or hypotensive patients with preexisting renal disease or in those receiving multiple nephrotoxic drugs is the most effective way to reduce nephrotoxicity. Acute interstitial nephritis is an immune process that is most commonly caused by penicillins, diuretics, allopurinol, nonsteroidal anti-inflammatory drugs, cimetidine, and sulfonamides. Prompt recognition of the disease and cessation of the responsible drug are usually the only necessary therapy. Chronic interstitial nephritis is most often seen after prolonged use of several different types of analgesic agents, including aspirin, acetaminophen, and nonsteroidal anti-inflammatory drugs. These patients develop recurrent papillary necrosis and eventually chronic renal failure. They are also at risk of developing transitional cell carcinomas of the urinary collecting system. Some patients who are receiving cyclosporine also develop chronic renal failure due to interstitial fibrosis.

Acute Kidney Injury↗
PubMed1990

The hepatorenal syndrome.

HRS occurs frequently in patients with advanced cirrhosis of the liver and fulminant hepatitis. The pathogenesis of HRS is not clearly understood; reduced effective plasma volume and intense renal cortical vasoconstriction seem to have important roles. The HRS is a diagnosis by exclusion, and it [table: see text] is often difficult to differentiate this entity from prerenal azotemia and ATN. The HRS is characterized by its relentless progression and usually fatal outcome. The essential steps in the management of HRS are to identify and correct the precipitating factors leading to HRS and avoidance of potential hepatotoxic and nephrotoxic drugs. Patients with potentially reversible liver diseases should be treated aggressively. Volume expansion is important and should be tried first, even though hypovolemia may be not clinically evident. Dialysis may benefit patients with fluid overload and electrolyte imbalance or those awaiting liver transplantation. In selective cases, peritoneovenous shunt may be of value. Liver transplantation is the only curative therapy available at present.

Animals↗
PubMed1986

Portal-systemic encephalopathy and hepatic coma.

Decompensation in the cirrhotic patient is typically manifested as hepatic encephalopathy or coma. This may be precipitated by azotemia, gastrointestinal bleeding, infection, hypokalemic alkalosis, excess dietary protein, or the use of sedative, tranquilizer, or analgesic medications. The pathogenesis of hepatic encephalopathy associated with portal-systemic shunting is unknown, but theories purporting major roles for ammonia, AAAs, false neurotransmitters, and GABA have been advanced. Treatment is aimed at removing precipitating factors and eliminating nitrogenous substances from the gastrointestinal tract.

Amino Acids↗
PubMed1980

Acute renal failure in cardiovascular and other surgical patients.

The acute onset of oliguria and azotemia in the postoperative setting may be caused by prerenal or postrenal causes or intrinsic renal damage. The first step in arriving at a diagnosis is to review the history in order to elicit the extrarenal factors. Certain simple laboratory tests are of tremendous value in differentiating these conditions. The development of acute renal failure with renal parenchymal damage usually occurs in the setting of hypotension, sepsis, dehydration, and with exposure to nephrotoxins. Most patients will be excreting scant amounts of isotonic urine containing more than 20 to 30 mEq per liter of sodium. Their urine:plasma creatinine ratio is less than or equal to 20:1 and their urinary sediment reveals many epithelial cells and casts. The condition is usually reversible and the treatment is expectant. However, it is still associated with a high mortality, although the survival of patients with acute renal failure may be substantially higher than previously reported. Early dialysis and nutritional support may play an important role in the improved survival. Patients with nonoliguric acute renal failure have urine outputs that may exceed 2 liters per day. Despite this output they demonstrate a stepwise increase in serum urea and creatinine. Urine sodium and osmolality are not very helpful. Many such patients do have low (less than 20 mEq per liter) urine sodium concentration and excrete isotonic urine.

Acute Kidney Injury↗
PubMed1982

Acute renal failure and renal tubular squamous metaplasia following treatment with streptozotocin.

Nephrotoxicity, in the form of transient proteinuria, azotemia, abnormalities of tubular function, and acute renal failure, is the major toxic condition following administration of streptozotocin. The renal morphologic and ultrastructural abnormalities associated with streptozotocin remain poorly defined. We describe a patient with metastatic islet cell tumor of the pancreas who was treated with 16 weekly courses of 1 g/m2 of streptozotocin without marked change in renal function. Following a six-week hiatus without change in renal function, a single course of 1 g/m2 of streptozotocin was administered and resulted in acute renal failure. Light microscopic examination of the kidneys showed irregularly dilated renal tubules lined by low cuboid epithelium. The cells were pleomorphic and showed some mitoses. Nuclei were irregular and variably hyperchromatic. Electron microscopic examination disclosed large aggregates of fine microfilaments in the proximal convoluted tubules and collecting ducts. Microfilament aggregates were both free in the cytoplasm and membrane bound. Microfilaments were proved to be tonofilaments by the demonstration of keratin within the epithelium, using the immunoperoxidase method. These data suggest that squamous metaplasia may be an important part of streptozotocin renal toxicity, and the suggestion is made that they may be an antecedent of neoplastic change.

Acute Kidney Injury↗