Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The early metabolic events in 33 patients with non-Hodgkin lymphoma were analyzed in the present study. Twenty-three patients had Burkitt lymphoma, 3 had non-Burkitt undifferentiated lymphoma and 7 had lymphoblastic lymphoma. Eight patients developed azotemia prior to starting chemotherapy while five did so during the first treatment week. All the patients but two who developed azotemia had stage C or D disease. Serum LDH prior to chemotherapy correlated well with the stage of disease and predicted the serum levels of creatinine, uric acid and phosphorus in the post-treatment period. Surgical excision of the main tumor mass was associated with a low incidence of azotemia and other metabolic derangements. Hyperuricemia and occasionally obstruction were encountered as the causes of azotemia in the pre-treatment period. Hyperuricemia and/or hyperphosphatemia were presumed responsible for the development of azotemia in the post-chemotherapy period. Two patients were dialyzed for renal failure due to hyperuricemia and one for renal failure due to hyperphosphatemia which developed shortly after starting chemotherapy. The patterns of renal and metabolic disturbances observed during treatment of these patients were characterized by the following profiles: 1. Azotemia due to hyperuricemia prior to treatment. 2. Hyperuricemia without azotemia in the pre-treatment period with azotemia due to hyperphosphatemia in the post-treatment period. 3. Azotemia due to combined hyperphosphatemia and hyperuricemia developing gradually in post-treatment period. 4. Increased urine phosphorus excretion in both non-azotemic and azotemic patients.
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PMID:Renal and metabolic complications of undifferentiated and lymphoblastic lymphomas. 689 77

This paper has outlined the varied renal and metabolic abnormalities which may occur as complications of antineoplastic chemotherapy. Rapid tumor lysis leading to acute uric acid nephropathy, hyperkalemia and hyperphosphatemia may complicate the treatment of patients with chemotherapy-responsive tumors. Aggressive management with intravenous hydration, urinary alkalinization and administration of allopurinol can ameliorate these complications of therapy. Many commonly used antineoplastic agents, particularly cisplatin, methotrexate, streptozotocin, and nitrosoureas, are nephrotoxic. Careful monitoring of renal function and serum electrolytes are essential during administration of these agents. In addition, intravascular volume depletion, urinary tract infection, and obstructive uropathy must always be considered when renal function deteriorates in patients with cancer. With foresight and aggressive management, many of these derangements can be ameliorated or avoided entirely and the toxicity of effective cancer chemotherapy can be minimized. Patients with established renal failure who require chemotherapy pose a particularly difficult clinical problem. Though a complete discussion of this subject is beyond the scope of this paper, Table 3 is included to provide some guidelines for dose modification in patients with altered renal function.
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PMID:Renal and metabolic toxicities of cancer chemotherapy. 720 Feb 63

Renal and metabolic complications of tumor lysis during 46 episodes of remission induction chemotherapy were reviewed in 37 patients with American Burkitt's lymphoma. Azotemia occurred in 14 patients, preceding chemotherapy in eight. All of these patients had abdominal tumors. Pretreatment azotemia was associated with elevated lactic dehydrogenase (LDH) and uric acid levels, and sometimes extrinsic ureteral obstruction by tumor. Two patients required dialysis for uric acid nephropathy before chemotherapy was initiated. Following chemotherapy, major complications of tumor lysis (hyperuricemia, hyperkalemia and hyperphosphatemia) were associated with very large tumors, high LDH levels and inadequate urinary output. In patients undergoing diuresis and receiving allopurinol, hyperkalemia or hyperuricemia developed infrequently unless concomitant renal failure ensued. Hyperphosphatemia, which occurred only after chemotherapy, developed in 10 of 32 (31 per cent) nonazotemic and in all azotemic patients. Hemodialysis was required in three post-treatment patients for control of azotemia, hyperuricemia, hyperphosphatemia and/or hyperkalemia. Because of the potential for renal failure caused by precipitation of phosphate, severe hyperphosphatemia is an additional criterion for dialysis in patients with acute tumor lysis syndrome.
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PMID:Acute tumor lysis syndrome. A review of 37 patients with Burkitt's lymphoma. 736 30

Deficiency of 1,25-dihydroxyvitamin D plays an important role in the pathogenesis of secondary hyperparathyroidism. Adequate replacement of this hormone is required to normalize parathyroid gland function and restore bone homeostasis in patients with advanced renal failure. Controversy exists regarding the best method of administering 1,25-dihydroxyvitamin D. Although initial, uncontrolled clinical trials suggested the superiority of intravenous calcitriol treatment, more recent controlled investigations have shown that different routes (oral versus intravenous), frequency (daily versus intermittent) and dosing (physiologic versus pharmacologic) of calcitriol administration are equivalent. Overall, the response to calcitriol treatment depends more on the severity of secondary hyperparathyroidism and the presence of confounding variables, such as hyperphosphatemia and acquired abnormalities of parathyroid cell function, than on the method of calcitriol administration.
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PMID:Oral versus intravenous calcitriol: is the route of administration really important? 755 95

Acute exertional rhabdomyolysis is caused by a skeletal muscle injury that results in the release of myoglobin and other cellular contents into the circulatory system. Recent reports suggest that acute exertional rhabdomyolysis is more common and more serious than previously realized. Mild to moderate acute exertional rhabdomyolysis can result in hyperkalemia, hypernatremia, lactic acidosis and hyperphosphatemia. Disseminated intravascular coagulation, renal failure and compartmental syndrome may also occur. The physician should maintain a high index of suspicion for acute exertional rhabdomyolysis in patients who present with symptoms of an overexertion injury, most commonly pain and swelling in the affected muscles. Special attention should be given to evaluating the history for occupational, recreational, environmental and medical risk factors for rhabdomyolysis. Screening may be performed with a simple urine dipstick test; if the urine is orthotoluidine-positive, the diagnosis should be confirmed with measurement of the serum creatine kinase level. Early intervention with aggressive hydration and close monitoring for metabolic, renal or hematologic complications may prevent serious injury or death.
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PMID:Acute exertional rhabdomyolysis. 762 24

Our understanding of the mechanism responsible for secondary hyperparathyroidism (HPTH) has advanced significantly since the "trade-off" hypothesis was formulated. It appears that in early renal failure a deficit of calcitriol synthesis is an important factor. However, additional factors, such as a defect of the vitamin D receptor or the newly cloned calcium sensor receptor (BoPCaR1), may be present in the parathyroid cells. As renal failure progresses, the lack of calcitriol becomes more pronounced, inducing HPTH. With advanced chronic renal failure, hyperphosphatemia is an additional important factor in worsening HPTH. In addition, resistance of the parathyroids to calcitriol due to a reduced density of calcitriol receptors also may contribute to HPTH. Finally, uremia per se not only may cause a receptor abnormality in the parathyroid but at the level of the bone it may aggravate the impaired calcemic response to PTH. In conclusion, after reviewing the "trade-off" hypothesis, although some of the original concepts may have been simplistic, most of the factors postulated 30 years ago are still operative in the pathogenesis of secondary HPTH in renal failure.
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PMID:Secondary hyperparathyroidism in renal failure: the trade-off hypothesis revisited. 774 20

Modern therapeutic concepts of chronic renal insufficiency are based on observations showing a retardation of progressive renal failure by therapeutic measures. In the context emphasis is now placed on the treatment of arterial hypertension and on the patient's adherence to a protein-restricted diet. In addition to these conservative measures it is important to avoid nephrotoxins, to hydrate the patient sufficiently and to treat advanced hyperlipidemias. Deficiencies of active vitamin D should be treated by oral vitamin D substitution after correction of hyperphosphatemia. In the treatment of the latter, preparations of calcium carbonate are now the preferred mode of treatment. In advanced renal insufficiency it is important to maintain a salt-restricted diet and to treat any attendant hyperkalemia and hyponatremia.
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PMID:[Conservative treatment in chronic kidney insufficiency]. 778 98

We encountered 5 cases of primary hyperparathyroidism (PHPT) accompanied by chronic renal failure over the past 4 years. Neither hypocalcemia nor hyperphosphatemia was found in the past records. The parathyroid hormone (PTH) levels in these cases were extraordinarily higher than those in usual patients suffering from renal failure. The manifestation of PHPT-developed insidiously together with the decline of renal function. Serum 1,25(OH)2D3 levels were lower than normal range in all cases, and which in turn might accelerate the progression of PHPT in a similar way as the development of secondary hyperparathyroidism. Parathyroidectomy (PTX) was done successfully in 4 cases, and the pathology of the biggest gland was adenoma but hyperplasia was found in other glands simultaneously. These results revealed the polymorphism of parathyroid glands in case of complication with renal failure. Furthermore, the interruption of postoperative 1 alpha(OH)D3 treatment induced the relapse of hyperparathyroidism (HPT). The case which refused PTX was treated by oral pulse therapy with 1,25(OH)2D3. The calcium/intact PTH sigmoidal curve examined 3 years later revealed that the set point shifted to right and upward despite therapy. It suggested that functional parathyroid mass became larger and the sensitivity to calcium became less under continuous stimuli on parathyroid glands. According to these results, PHPT accompanying with renal failure is resistant to medical therapy, and surgical treatment is a possibility. In this occasion, total PTX with autograft transplantation is better than simple adenectomy because even the glands not responsible to clinical manifestation of PHPT can have some pathological abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical profile and outcome of primary hyperparathyroidism accompanied by chronic renal failure. 785 Oct 33

A total of 126 (99 males, 27 females) serologically confirmed hospital-treated adult cases of nephropathia epidemica (NE) were studied. The initial diagnosis suggested by the referring physician was correct in only 28%. Some rare clinical manifestations of NE were observed; acute myopericarditis in 3 patients and encephalitis in 1. Pulmonary involvement due to vascular congestion was observed in 16% and liver involvement in 34% of the patients. Thrombocytopenia was present in 75%, leukocytosis in 50% and anemia in 50%. Erythrocyte sedimentation rate (ESR) was 2-108 (mean 38) mm/h and C-reactive protein (CRP) 0-126 (mean 52) mg/l. Proteinuria was observed in 94%, hematuria in 58% and pyuria in 28%. Electrolyte abnormalities (hyponatremia, hypokalemia, hypocalcemia, hyperphosphatemia) were all common but rarely serious. Serum lipid changes caused by the acute infection and renal failure included very low total and HDL-cholesterol as well as high triglyceride levels. Renal function was transiently impaired in 94% of the patients and 7 needed transient dialysis therapy. All recovered.
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PMID:Nephropathia epidemica in Finland: a retrospective study of 126 cases. 791 Jul 5

To examine the most effective route (intravenous vs. "pulse" oral), dose (physiologic vs. pharmacologic) and long-term efficacy of calcitriol therapy for secondary hyperparathyroidism in patients with end-stage renal disease (ESRD), we randomized 19 hemodialysis patients with severe hyperparathyroidism to receive over a 36-week study period either pulse orally administered calcitriol and intravenous placebo (pulse oral group; N = 9) or intravenous calcitriol and oral placebo (intravenous group; N = 10). Calcitriol was given intermittently in a double-blinded fashion at an initial dose of 2 micrograms thrice weekly and increased as tolerated up to a maximum dose of 4 micrograms per treatment. All patients received similar daily calcium supplementation (2.5 g of elemental calcium) and low dialysate calcium (1.25 mmol/liter) throughout the study period. At the maximum tolerated calcitriol dose, serum 1,25-dihydroxyvitamin D levels were significantly greater 60 minutes following intravenous (389 pmol/liter) compared to oral administration (128 pmol/liter). In spite of the different pharmacologic profiles, intravenous and oral administered calcitriol resulted in similar reductions of serum PTH over the 36 week period of observation (P = 0.300), achieving an overall maximum average PTH reduction of 43% (P = 0.016). Long-term intensive calcitriol therapy (independent of administration route), however, failed to decrease parathyroid gland size as assessed by high resolution ultrasound and/or magnetic resonance imaging. Calcitriol therapy also failed to alter the calcium sensitivity as assessed by serial PTH measurements in response to calcium loading. Increases in serum calcium, but not calcitriol dose or parathyroid gland size, predicted decrements in serum PTH, whereas hyperphosphatemia and the level of PTH suppression derived from the PTH/ionized calcium response curves predicted refractoriness to calcitriol therapy. Episodes of hypercalcemia and hyperphosphatemia were similar in both treatment groups and limited the dose of calcitriol that could be administered. These data indicate that intermittent intensive calcitriol therapy, regardless of administration route, is poorly tolerated, fails to correct parathyroid gland size and functional abnormalities, and has a limited ability to achieve sustained serum PTH reductions in end-stage renal failure patients with severe hyperparathyroidism.
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PMID:Prospective trial of pulse oral versus intravenous calcitriol treatment of hyperparathyroidism in ESRD. 793 19


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