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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.
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PMID:Drug-induced renal disease. 38 1

A family is reported where four males have developed hyperuricemia, renal damage and, except for the youngest person affected, gout at an early age. The disease appears to be inherited as an X-linked recessive metabolic error. Clinically the patients have developed classical, tophaceous gout before the age of 25 and have suffered repeated attacks of renal colic. Renal tubular damage with decreased ability to concentrate and acidify urine was seen in a family member of only 16 years of age. Progressive renal failure seems to develop slowly. None in the family has shown neurologic symptoms, and two of the four affected men are apparently of at least average intelligence, two slightly below average. One female carrier has repeatedly passed uric acid stones. Studies of the red blood cell lysate have shown a normal activity of enzyme hypoxanthine phosphoribosyltransferase, and an increased level of adenine phosphoribosyltransferase. Skin fibroblasts from affected family members grew normally in the presence of 8-azaguanine. Administration of azathioprine to the patients did not decrease their serum uric acid levels. This is the first family described with this type of disorder of the purine metabolism.
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PMID:Recessive X-linked hyperuricemia with gout and renal damage, normal activity of hypoxanthine phosphoribosyltransferase and resistance to azaguanine. 42 44

The authors observed 812 patients with nephrolithiasis who underwent 876 sessions of shock-wave lithotripsy on Sonolith-3000 lithotriptor supplied with an ultrasonic system of the stone localization. The size of nephroliths ranged from 0.7 to 4.2 cm. Large-size nephroliths required repeated sessions and pretreatment establishment of the stent. The procedure proceeded without anesthesia. Subsequent renal colic was reported in 126 (15.5%), an exacerbation of pyelonephritis in 45 (5.5%), subcapsular hematoma in 4 (0.5%) of the patients. 790 patients showed clinical response (97.3%), with a complete destruction of the stone in 446 (54.9%) and partial one in 344 (42.4%) cases. 27 subjects were treated in outpatient setting. According to the authors, lithotripsy is contraindicated in urinary tract obstruction below the stone, renal failure, chronic pyelonephritis in the active phase of inflammation, marked impairment of cardiac rhythm.
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PMID:[Extracorporeal shockwave lithotripsy on the Sonolith-3000 apparatus]. 175 17

We report a case of homozygous adenine phosphoribosyl transferase (APRT) deficiency associated with 2,8-dihydroxyadenine stones recurrent in a patient with a renal transplant. The disease was diagnosed 23 years after the initial episode of renal colic. At that time the disease was unknown. Our patient is only the second case of this disorder reported from the United States. Correct diagnosis is important because long-term maintenance with allopurinol and a low purine diet can effectively prevent stone formation and renal failure.
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PMID:2,8-dihydroxyadenine urolithiasis: report of a case first diagnosed after renal transplant. 307 70

The management of the patient presenting to the Emergency Department with nephrolithiasis or renal colic should include evaluation of the patient for concurrent diseases, risk factors for stone formation, and possible etiologies for stones. Suspicion of ureterolithiasis is based on a cogent history and physical examination and reinforced by a finding of hematuria. Diagnosis should be based upon a promptly performed intravenous pyelogram, unless the patient is truly allergic to contrast media or has substantial risk of a contrast-induced renal failure. A solitary flat plate of the abdomen adds no useful information and is an unnecessary expense to the patient. Essential laboratory data include a urinalysis, CBC, and electrolyte, BUN, creatinine, and serum calcium levels. A urine culture should be obtained in all patients because urinalysis alone may not be sufficient to exlude a urinary tract infection. Initial treatment of the patient with an uncomplicated renal colic should include hydration, relief of pain, and reassurance. Evaluation by a consultant may be done as an outpatient on a nonemergent basis. If the colic has not resolved after 72 hours, hospitalization generally is recommended. If the patient has vomiting, dehydration, a complete obstruction, or a solitary kidney, hospitalization in indicated and urgent consultation recommended. If the patient has fever or other signs of infection, emergent consultation and immediate hospitalization are essential. Retained obstructing stones are generally managed by urologic consultants. It is in the care of the patient with the retained stone that greatest advances have been made in the past 10 years. Patients should be counseled that the retained stone no longer calls for extended hospitalization and convalescence.
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PMID:Nephrolithiasis. 329 30

A 45-year-old man with the Acquired Immunodeficiency Syndrome (AIDS) and CNS toxoplasmosis presented with acute renal failure, hematuria, and renal colic shortly after starting treatment with sulfadiazine. Ultrasound examination of his kidneys was suggestive of intraparenchymal crystallization of sulfadiazine. His renal failure and ultrasound findings rapidly resolved with alkaline hydration. On rechallenge with sulfadiazine, he again developed renal insufficiency and ultrasonic findings consistent with stones. The use of sulfadiazine in the treatment of CNS toxoplasmosis in AIDS patients should be monitored carefully with the recognition that this form of crystalline-induced acute renal failure can occur in a dehydrated patient.
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PMID:Sulfadiazine-associated obstructive nephropathy occurring in a patient with the acquired immunodeficiency syndrome. 338 58

Renacidin is a urinary stone dissolving agent composed primarily of gluconic and citric acids and their magnesium salts, buffered to a pH of 4. We describe its use in a child with oxalosis, disabling renal colic and deteriorating renal function in whom its use was associated with hypermagnesemia and rapid progression of the renal failure. Possible mechanisms for the deterioration in renal function are discussed.
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PMID:Hypermagnesemia and progression of renal failure associated with renacidin therapy. 372 36

We evaluated the stone recurrence rate and long-term renal function in 50 patients with a solitary kidney 60 to 84 months (mean 70.6) after unilateral nephrectomy for urinary tract stone disease. Followup evaluation included a detailed history, physical examination, blood and urine biochemistry studies, urinalysis, urine culture, excretory urography, ultrasonography of the kidney and 131iodine-ortho-iodohippurate renography. The overall stone recurrence rate in unilateral nephrectomy urolithiasis patients was 30% (15 of 50). The mean interval until stone recurrence was 31.1 months (range 6 to 74) and the mean episodes of recurrence were 2.1 times per patient (range 1 to 5). Function of the remnant kidney in most patients was unchanged during followup. However, 2 of the 15 patients with recurrent stones had anuria during the acute attack of renal colic and, thus, required percutaneous nephrostomy urinary diversion, while 1 had proteinuria (3 gm. per day) and progressive renal failure 47 months after nephrectomy. The metabolic stone patients seemed to experience recurrence more easily than metabolic stone patients seemed to experience recurrence more easily than infection stone patients (37% versus 13%) but no statistically significant difference was noted (p = 0.198).
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PMID:The long-term stone recurrence rate and renal function change in unilateral nephrectomy urolithiasis patients. 793 65

The primary care physician has a responsibility not only to recognize and treat acute stone passage but to ensure that the patient with recurrent stones has metabolic evaluation and appropriate preventive care. Renal colic is typically severe, radiates to the groin, is associated with hematuria, and may cause ileus. About 90% of stones that cause renal colic pass spontaneously. The patient with acute renal colic should be treated with fluids and analgesics and should strain the urine to recover stone for analysis. Highgrade obstruction or failure of oral analgesics to relieve pain may require hospitalization; a urinary tract infection in the setting of an obstruction is a urologic emergency requiring immediate drainage, usually with a ureteral stent. Several approaches are available when stones do not pass spontaneously, including extracorporeal shock wave lithotripsy, percutaneous lithotripsy, and ureteroscopic laser lithotripsy. Calcium stone disease has a lifetime prevalence of 10% in men and causes significant morbidity. Renal failure is unusual. Stone types include calcium oxalate, uric acid, struvite, and cystine. Stone analysis is particularly important when a noncalcareous constituent is identified. The majority of patients with nephrolithiasis will have recurrence, so prevention is a high priority. High fluid intake is a mainstay of prevention. Metabolic evaluation will indicate other appropriate preventive measures, which may include dietary salt and protein restriction, and use of thiazide diuretics, neutral phosphate, potassium citrate, allopurinol, and magnesium salts. Dietary calcium restriction may worsen oxaluria and negative calcium balance (osteoporosis).
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PMID:Nephrolithiasis: acute management and prevention. 965 69

Analgesic nephropathy is a slowly progressive disease caused by the chronic abuse of analgesic mixtures containing two analgesic components combined with potentially addictive substances (coffeine and/or codeine). Pathologically, the nephropathy is characterized by renal papillary necrosis with calcification and chronic interstitial nephritis sometimes in association with transitional-cell carcinoma of the uroepithelium. In the early stage, the clinical characteristics are polyuria, sterile pyuria, sometimes renal colic and haematuria. With further progression of the disease, there are the nonspecific symptoms of advanced renal failure. The incidence of classic analgesic nephropathy among Hungarian patients on chronic renal replacement therapy has proven. There is an urgent need for the estimation of analgesic nephropathy among patients with chronic renal disease and among patients with chronic pain presumably regularly taking analgesics in Hungary. As long as analgesic mixtures containing phenacetin or paracetamol and/or nonsteroidal antiinflammatory drugs and addictive substances are available "over-the-counter", analgesic nephropathy will continue to be a problem also in our country.
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PMID:[Analgesic nephropathy]. 984 64


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