Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four patients of pure gouty nephropathy are presented. Gout was of over five years duration and asymptomatic nephropathy manifested as non-oliguric acute renal failure. Diseases commonly associated with it like uric acid stones, urinary tract infections, hypertension, diabetes mellitus, hyperlipidemid, obesity and nephrosclerosis were absent. Reduction in serum uric acid level resulted in prompt improvement in renal functions. Early detection and control of hyperuricemia may help in restoration of renal functions.
 ...
PMID:Non-oliguric acute renal failure in gout. 139 13

One way to prevent chronic renal failure (CRF) is to institute preventive measures against renal diseases in the general population. Patients with hereditary kidney diseases should have genetic counselling. Certain infections affecting or causing kidney diseases can be eradicated. People should be cautious in the use of analgesics and non-steroidal anti-inflammatory agents. Exposure to hydrocarbons, heavy metals and toxic gases should be avoided. Proper management of diabetes mellitus, gout, renal stones and hypertension can prevent renal damage. In patients with established renal disease, the following factors if treated or modified can prevent or ameliorate renal injury: glomerular hypertension, cell mediated proliferation, lipid induced proliferation, coagulation and thrombosis. Pregnancy in patients with renal disease should be well managed and termination advised if necessary. Reversible causes of renal failure as well as acute reversible elements can be removed or treated. Acute renal failure due to toxins can be avoided, although prevention requires awareness of association with renal failure. Prevention too depends on early detection of nephrotoxic injury like: greater awareness of hazards of environmental toxins, careful monitoring of dosage of nephrotoxic drugs and when possible, total avoidance of nephrotoxins should be the rule. Finally, in patients with glomerular disease, prevention or amelioration of glomerular damage with pharmacological agents have been achieved in some instances.
 ...
PMID:Can therapeutic interventions prevent chronic renal failure? 141 97

The best definition of risk factors for renal injury, irrespective of the aetiological agent, comes from observations in patients with acute renal failure. From such observations, two subdivisions have evolved, i.e., acute insults and host risk factors. Acute renal insults include: hypertension, sepsis, use of nephrotoxic drugs (e.g., aminoglycoside antibiotics and contrast media), haemoglobinuria or myoglobinuria, liver disease and extracellular volume depletion. Host risk factors include: advanced age, hypertension, gout and hyperuricaemia, diabetes mellitus, chronic renal failure and use of diuretics. Furthermore, the mechanism of acute renal injury can be correlated with different risk factors: for a tubular toxic agent, acting either directly on the cells or haemodynamically, a dose-dependency is characteristic; while for immunologically mediated injury, genetic predisposition is more important. The identification of risk factors for chronic toxic injury is confounded by the possibilities of multiple episodes of subclinical renal injury, the distinct possibility that a major component of the ageing process may be a loss of renal reserve, and a progressive body burden, of, e.g., cadmium, which may deplete intrinsic protective mechanisms. However, clinically relevant risk factors can alert the clinician to exercise additional caution when prescribing medications that are potentially nephrotoxic. Such factors include dehydration, pre-existing renal disease, age, co-existing diseases that cause renal ischaemia, gender, concomitantly administered drugs, and electrolyte abnormalities.
 ...
PMID:Risk factors for toxic nephropathies. 265 33

Accepted causes (acute insults) and risk factors for the development of acute renal failure were defined, quantitatively assessed, and tested for statistical significance in 143 patients with acute tubular necrosis. Sixty-two percent of patients had more than one acute insult, and 48 percent had more than one suspected risk factor. Hypotension, excessive aminoglycoside exposure, pigmenturia, and dehydration were identified as highly significant acute insults, while it was concluded that sepsis and administration of radiocontrast material could not be incriminated as causes of acute tubular necrosis. An additive interaction between acute insults was demonstrated, and the severity of acute renal failure was related to the number and severity of acute insults. Patients with oliguric renal failure had more severe acute insults than patients with nonoliguric renal failure. Preexisting renal disease and chronic hypertension were significant risk factors, the latter only when hypotension had been one of the acute insults. An age of more than 59 years, gout and/or chronic hyperuricemia, diabetes, and long-term diuretic administration were not found to be significant risk factors.
 ...
PMID:Acute renal failure. Multivariate analysis of causes and risk factors. 711 78

Recombinant myeloid growth factors have been increasingly used in recent years to combat induced and disease associated neutropenia. Their application in the management of Felty's syndrome with intercurrent infection has raised concern that resultant neutrophilia and activation of a diverse array of polymorphonuclear cell functions may have an adverse effect on the rheumatoid disease process. We describe a patient with Felty's syndrome receiving short term treatment with recombinant human granulocyte colony stimulating factor (GCSF), who then developed acute renal failure in conjunction with leukocytoclastic vasculitis and presumptive gout. We address the issue of "adding fuel to the fire" and review reported implications of GCSF in induction of vasculitis.
 ...
PMID:Vasculitis complicating granulocyte colony stimulating factor treatment of leukopenia and infection in Felty's syndrome. 754 56

Gout in heart transplant recipients is common and poses a significant therapeutic challenge. Concomitant administration of azathioprine and allopurinol therapy carries a high risk of leukopenia. Uricosuric agents can cause renal lithiasis and/or acute renal failure in patients with renal failure and/or high urinary levels of uric acid. We report our experience with urate-oxidase in three heart transplant recipients with severe polyarticular and tophaceous gout, a history of leukopenia under allopurinol and unresponsiveness or contraindications to uricosuric agents. Urate-oxidase was given parenterally in a dosage of 1000 units per day, seven days a month. The injections were done intramuscularly in one patient and intravenously in the other two, who were under anticoagulant therapy. Patients 1 and 2 received 12 and 6 courses, respectively. The third patient had had four courses and was still under treatment at the time of this writing. Shrinking of the tophi and improved mobility of the fingers were seen in all three patients after the second course. No adverse effects were recorded. Our experience suggests that urate-oxidase therapy may decrease the urate burden in patients with severe tophaceous gout. Urate-oxidase therapy should be viewed as a phase in the treatment of gout, which must be followed by administration of another agent.
 ...
PMID:Urate-oxidase for the treatment of tophaceous gout in heart transplant recipients. A report of three cases. 765 72

A 20-day-old male infant presented with acute renal failure. Three weeks later he developed acutely swollen, hot, red joints and tophi in his hands and feet. The serum uric acid was 2.2 mmol/l (normal 0.13-0.23 mmol/l) and the urinary oxypurine/creatinine ratio was 2.26 mmol (normal < 1.5 mmol). Complete deficiency of hypoxanthine guanine phosphoribosyl transferase (HGPRT) in intact erythrocytes confirmed Lesch-Nyhan syndrome. Neurological development was delayed and self-mutilation was observed at 22 months. Acute renal failure secondary to crystal nephropathy and tophaceous gout are unusual presenting features of this rare condition. This child also had transient neonatal hypothyroidism, which is not a recognized manifestation of the syndrome.
 ...
PMID:Lesch-Nyhan syndrome presenting with renal insufficiency in infancy and transient neonatal hypothyroidism. 815 15

Lead intoxication in human beings has been documented since the second century B.C. Renal disease, hypertension, and gout have all been linked to lead by strong circumstantial evidence. Both acute and chronic nephropathy can occur as a result of lead poisoning. Acute renal failure develops following acute lead intoxication and is often associated with gastrointestinal, neurologic, and hematologic disorders. Both blood and urinary laboratory abnormalities are associated with acute intoxication and are often diagnostic. Chronic lead nephropathy, a chronic tubulointerstitial nephritis on biopsy, occurs in the setting of long-term lead exposure and is often associated with hypertension and gout. Diagnosis of chronic lead nephropathy is more difficult since the laboratory abnormalities seen with acute lead intoxication are not present with chronic lead exposure. The typical clinical picture and the exclusion of other causes of renal disease allow the diagnosis of chronic lead nephropathy to be made. Evaluation of lead stores by either the calcium disodium edetate (EDTA) mobilization test or K-x-ray fluorescence are helpful in clinching the diagnosis. Treatment with EDTA lead mobilization is effective for acute lead poisoning while avoidance of further lead exposure prevents recurrence of lead intoxication. Treatment of chronic lead nephropathy with EDTA lead mobilization is useful if renal failure is modest; however, EDTA mobilization is of no benefit in patients with more severe renal insufficiency.
 ...
PMID:Lead and the kidney: nephropathy, hypertension, and gout. 890 77

The risk for renal insufficiency by uric acid precipitation in medulla of kidney correlates with the degree of uric acid supersaturation in the urine, depending on uric acid concentration and urinary pH. The patients with gout or hyperuricemia have sometimes acidic urine and increased uric acid excretion. Accordingly, these patients frequently accompany by renal insufficiency. Improvement of hyperuricosuria, increasing of urine volume, and alkalinization of urine to pH6 6.5, are effective for the prevention from renal insufficiency. Acute renal failure related to hyperuricemia, can also occured secondary to cell lysis. Tumor lysis syndrome is a critical illness characterized by massive tumor cell death leading to severe hyperuricemia, hyperphosphatemia, hypocalcemia, and acute renal failure after starting chemotherapy to cancers, especially lymphoproliferative malignancies. Administration of allopurinol 500-600 mg and adequate hydration and alkalinization of urine are advocated to prevent acute renal failure. Intensive care with hemodialysis is often required to treat renal failure, because renal failure is reversible in most cases.
 ...
PMID:[Hyperuricemia and the kidney]. 897 5

The present review summarizes the current knowledge on the multiple effects of alcohol overconsumption on the kidney function as well as on water, electrolyte and acid-base homeostasis. In contrast to the well known transitory diuretic effects, the overall long-term effect of chronic alcohol overconsumption is water and salt retention with expansion of extracellular volume. Furthermore, depletion of magnesium, phosphate and calcium is also frequently found in alcohol-dependent patients. These electrolyte disturbances may be associated with the alcohol-induced hypoparathyroidism and parathyroid hormone resistance of the skeletal muscle as well as with the decrease of serum osteocalcin. Metabolic acidosis with lower arterial blood pH and plasma bicarbonate concentrations was revealed in alcoholic patients upon admission and a significant correlation between chronic alcohol overconsumption and increased incidence of hyperuricemia and gout attacks was also reported. Alcohol seems to have dual effects on the blood pressure. Increased blood pressure was demonstrated in men above 80 g and in women above 40 g ethanol consumption daily. In contrast, young adults consuming only 10 to 20 g per day had lower blood pressure than the abstinent group indicating a J-curve relationship. This is in line with the lowered risk for coronary heart disease associated with regular consumption of small alcohol amounts. The mechanisms responsible for the association between alcohol overconsumption and postinfectious glomerulonephritis have not been elucidated yet. Finally severe alcohol abuse predisposes to acute renal failure and seems to be associated with the general catabolic effects.
 ...
PMID:Alcohol abuse: potential role in electrolyte disturbances and kidney diseases. 987 14


1 2 3 Next >>