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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article includes a review of hypertension, nephrolithiasis and cystic diseases of the kidney, all quite common diagnoses. These days, as concerns are growing, some are considering diabetes mellitus to be a national epidemic. Thus, our entire article focuses on the diabetic renal disease. The current approach to the diagnosis and treatment of acute renal failure and chronic renal insufficiency is discussed, including treatment modalities such as dialysis and transplantation. This article is not at all intended to be a comprehensive review of each topic included, but rather it is an attempt to make the reader more familiar with the fascinating and continuously evolving field of nephrology.
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PMID:Updates in nephrology. A summary of common diagnoses encountered in the clinical practice. 1180 65

Fungal urinary tract infections are an increasing problem in hospitalized patients. Funguria may be a result of contamination of the urine specimen, colonization of hte urinary tract, or may be indicative of true invasive infection. In this study, we report the risk factors, clinical features, treatments and outcome in a group of 68 hospitalized patients (adults and children) with fungal isolates recovered from 103 urinary samples. Underlying medical conditions were present in most patients. In the pediatric group, urinary tract abnormalities (86%) and prematurity (19%)accounted for the majority of the cases. Diabetes mellitus (28%), nephrolithiasis, and benign prostatic hyperplasia were the most common diseases in adults. Indwelling urethral catheters were noted in 38% of the pediatric patients and in 43% of adults during hospitalization. Candida albicans strains were responsible for 97% and 75% of positive cultures in children and adults, respectively. Symptoms such as fever, dysuria, frequency and flank pain were generally absent in both groups. Fluconazole was the most frequent antifungal utilized (61%) in children and ketoconazole in the adult group (42%). Removing the urinary catheter was attempted in 6 pediatric patients (29%) and in only 8 adults (17%). One patient (4%) in the pediatric group died compared to 10 in the adult group (21%, p=0.04). Successful diagnosis and treatment of funguria depends on a clear understanding of the risk factors and awareness of fungal epidemiology.
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PMID:Hospital-associated funguria: analysis of risk factors, clinical presentation and outcome. 1198 May 93

We retrospectively analyzed the results of 75 living-related pediatric renal transplants performed at our center between January 1986 and December 1999. The major causes of end-stage renal disease (ESRD) were glomerulonephritis (26%) and nephrolithiasis (16%), while the etiology was unknown in 50%. The mean age of the recipients was 12 yr (range 6-17 yr) and that of the donors was 39 yr (range 20-65 yr). The majority (73%) of donors were parents. Eighty five per cent of donors were one-haplotype matched and the rest identical. Immunosuppression was based on a triple drug regimen. Thirty per cent of recipients were rapid metabolizers of cyclosporin A (CsA) (area under the curve [AUC]: < 6,000 ng/mL/h), while 16% were slow metabolizers (AUC: > 8,000 ng/mL/h). Forty three (57%) children encountered 59 rejection episodes, the majority of which (59%) were recorded in the first month post-transplant. Seventy-four per cent of the rejection episodes were steroid sensitive and the rest, except two, were resolved by therapy with antithymocyte globulin (ATG) or orthoclone thymocyte 3 (OKT3). After a mean follow-up of 37 months, 17 (22%) grafts had chronic rejection and 76% of these recipients had previously experienced acute rejection episodes. The overall infection rate was high, necessitating two hospital admissions/patient/year. The majority (53%) of the infections were bacterial. Urinary tract infections (UTIs) were seen in 17 (23%) recipients. Twelve of these had ESRD as a result of stone disease and eight grafts were lost because of UTIs. Eight per cent of recipients developed tuberculosis (TB), and extra-pulmonary lesions were seen in 50%. Surgical complications were encountered in eight patients. Free medication to all recipients and parental support ensured a compliance rate of 93%. Baseline growth deficit was seen in children of the two groups studied (the 6-12 yr and 13-17 yr age-groups), with Z-scores of - 2.39 and - 2.12, respectively. No growth catch-up was observed at 12 and 24 months in either group. Post-donation complications were seen most commonly in donors > 50 yr of age and included: proteinuria (> 300 mg/24 h, four patients), hypertension (three patients), and diabetes (one patient). Twenty-four grafts were lost, 54% as a result of immunological and the rest as a result of non-immunological causes, and 17 recipients died during the follow-up period. Infections were the main cause of patient and graft loss. Overall 1- and 5-yr graft and patient survival rates were 88% and 65%, and 90% and 75%, respectively.
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PMID:Living-related pediatric renal transplants: a single-center experience from a developing country. 1200 Apr 64

Recommendations for increased consumption of protein are among the most common approaches of popular or fad diets. This review summarizes the effects of dietary protein on satiety, energy intake, thermogenesis, and weight loss, as well as its effect on a variety of health outcomes in adults. In short-term studies, dietary protein modulates energy intake via the sensation of satiety and increases total energy expenditure by increasing the thermic effect of feeding. Whereas these effects did not contribute to weight and fat loss in those studies in which energy intake was fixed, one ad libitum study does suggest that a high-protein diet results in a greater decrease in energy intake, and therefore greater weight and fat loss. In terms of safety, there is little long-term information on the health effects of high-protein diets. From the available data, however, it is evident that the consumption of protein greater than two to three times the U.S. Recommended Daily Allowance contributes to urinary calcium loss and may, in the long term, predispose to bone loss. Caution with these diets is recommended in those individuals who may be predisposed to nephrolithiasis or kidney disease, and particularly in those with diabetes mellitus.
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PMID:High-protein weight-loss diets: are they safe and do they work? A review of the experimental and epidemiologic data. 1214 97

This cross-sectional cohort study of 5566 women and 2187 men 50 years of age and older in the population-based Canadian Multicentre Osteoporosis Study was conducted to determine whether reported past diseases are associated with bone mineral density or prevalent vertebral deformities. We examined 12 self-reported disease conditions including diabetes mellitus (types 1 or 2), nephrolithiasis, hypertension, heart attack, rheumatoid arthritis, thyroid disease, breast cancer, inflammatory bowel disease, neuromuscular disease, Paget's disease, and chronic obstructive pulmonary disease. Multivariate linear and logistic regression analyses were performed to determine whether there were associations among these disease conditions and bone mineral density of the lumbar spine, femoral neck, and trochanter, as well as prevalent vertebral deformities. Bone mineral density measurements were higher in women and men with type 2 diabetes compared with those without after appropriate adjustments. The differences were most notable at the lumbar spine (+0.053 g/cm2), femoral neck (+0.028 g/cm2), and trochanter (+0.025 g/cm2) in women, and at the femoral neck (+0.025 g/cm2) in men. Hypertension was also associated with higher bone mineral density measurements for both women and men. The differences were most pronounced at the lumbar spine (+0.022 g/cm2) and femoral neck (+0.007 g/cm2) in women and at the lumbar spine (+0.028 g/cm2) in men. Although results were statistically inconclusive, men reporting versus not reporting past nephrolithiasis appeared to have clinically relevant lower bone mineral density values. Bone mineral density differences were -0.022, -0.015, and -0.016 g/cm2 at the lumbar spine, femoral neck, and trochanter, respectively. Disease conditions were not strongly associated with vertebral deformities. In summary, these cross-sectional population-based data show that type 2 diabetes and hypertension are associated with higher bone mineral density in women and men, and nephrolithiasis may be associated with lower bone mineral density in men. The importance of these associations for osteoporosis case finding and management require further and prospective studies.
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PMID:Associations among disease conditions, bone mineral density, and prevalent vertebral deformities in men and women 50 years of age and older: cross-sectional results from the Canadian Multicentre Osteoporosis Study. 1267 40

The pathogenesis of nephrolithiasis in Cushing's syndrome is still not completely clarified. The current study aimed at investigating prevalence of nephrolithiasis and role of different lithogenic factors in Cushing's disease (CD). Forty-six CD patients (24 with active and 22 with cured disease) and 46 sex- and age-matched controls entered the study. Body mass index, blood pressure, fasting glucose and insulin, serum and urinary creatinine, urea, uric acid, electrolytes, and cystine, urinary volume, pH, oxalate, and citrate levels, and renal ultrasonography (US) were performed in all patients and controls. Nephrolithiasis was found in 50% of active patients, 27.3% of cured patients, and 6.5% of controls (P < 0.001). Compared with controls, patients with active disease had a significantly increased prevalence of obesity, arterial hypertension, diabetes mellitus, hypercalciuria, hypocitraturia, and hyperuricosuria, significantly higher levels of serum and urinary cystine, urinary creatinine, urea, uric acid, potassium, calcium, phosphorus, and oxalate, significantly lower levels of urinary citrate levels. Compared with controls, patients cured from CD had a significantly increased prevalence of obesity, systemic arterial hypertension, and diabetes mellitus, whereas urinary citrate was significantly decreased. At multivariate analysis, a significantly increased risk to develop kidney stones was independently associated with urinary excretion of uric acid (odds ratio = 1.6, confidence interval = 1.0-2.5) and systemic arterial blood pressure (odds ratio = 2.6, confidence interval = 1.1-6.6). In conclusion, patients with active CD have an increased prevalence of nephrolithiasis compared with general population, which decreases but not disappears in patients successfully cured from the disease. This complication is likely caused by the synergic effect of different hypercortisolism-dependent metabolic and hemodynamic abnormalities, among which systemic arterial hypertension and excessive urinary uric acid excretion seem to play a pivotal role.
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PMID:Nephrolithiasis in Cushing's disease: prevalence, etiopathogenesis, and modification after disease cure. 1272 57

Increasing prevalence of diabetes mellitus and rising patient life expectancy are causing an accumulation of urologic late complications-despite or due to steadily improving medical health care. The prevalence of diabetic cystopathy (impaired bladder sensation, increased bladder capacity, sometimes accompanied by voiding difficulties and residual urine) is 25% in non-insulin-dependent diabetics and 48% in insulin-dependent diabetics. Autonomic and peripheral neuropathy lead to detrusor hyposensitivity, and chronic overstretching of the bladder causes myogenic detrusor hypocontractility. Since diabetic cystopathy often develops insidiously and asymptomatically, prevention of secondary complications such as recurrent urinary tract infections, vesicorenal reflux, nephrolithiasis, and pyelonephritis requires the urologist's full attention as well as early and repeated urodynamic diagnostics. Comorbidities can lead to a variety of urodynamic findings. Therapeutic options are generally conservative (timed voiding, micturition training, CIC, pharmacotherapy) and should be part of an integrated interdisciplinary health care approach since undiscovered complications involving non-urologic organ systems create a higher long-term socioeconomic burden than preventive support provided by other specialists.
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PMID:[Diabetes mellitus and bladder function. What should be considered?]. 1466 81

CBS domains are defined as sequence motifs that occur in several different proteins in all kingdoms of life. Although thought to be regulatory, their exact functions have been unknown. However, their importance was underlined by findings that mutations in conserved residues within them cause a variety of human hereditary diseases, including (with the gene mutated in parentheses): Wolff-Parkinson-White syndrome (gamma 2 subunit of AMP-activated protein kinase); retinitis pigmentosa (IMP dehydrogenase-1); congenital myotonia, idiopathic generalized epilepsy, hypercalciuric nephrolithiasis, and classic Bartter syndrome (CLC chloride channel family members); and homocystinuria (cystathionine beta-synthase). AMP-activated protein kinase is a sensor of cellular energy status that is activated by AMP and inhibited by ATP, but the location of the regulatory nucleotide-binding sites (which are prime targets for drugs to treat obesity and diabetes) was not characterized. We now show that tandem pairs of CBS domains from AMP-activated protein kinase, IMP dehydrogenase-2, the chloride channel CLC2, and cystathionine beta-synthase bind AMP, ATP, or S-adenosyl methionine,while mutations that cause hereditary diseases impair this binding. This shows that tandem pairs of CBS domains act, in most cases, as sensors of cellular energy status and, as such, represent a newly identified class of binding domain for adenosine derivatives.
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PMID:CBS domains form energy-sensing modules whose binding of adenosine ligands is disrupted by disease mutations. 1472 9

DEFINITION OF HYPOURICEMIA: Hypouricemia (serum uric acid less than 120 micro mol/l) is a biological abnormality often discovered accidentally and with a low prevalence depending on its permanent or transitory nature ranging from 0.15 to 3.38%. NEW PHYSIOLOGICAL CONCEPTS OF ITS PATHOGENESIS: Recently, our knowledge of the physiopathological mechanisms of hypouricemia has been emphasized by the identification of three systems of renal and extra-renal uric acid transport: a Cl/urate (URAT1) transporter, a multispecific organic anion transporter (OAT) and a urate transporter/channel. ETIOLOGY AND COMPLICATIONS OF HYPOURICEMIA: Through questioning, drugs and toxics (allopurinol.) are generally rapidly recognized as responsible for half of the hypouricemia encountered. It can be concomitant to a known disease: severe liver disease, neoplasia, diabetes, AIDS, syndrome of inappropriate antidiuretic hormone secretion. Hypouricemia can also be isolated and justifies the measurement of uric acid clearance, the normality or reduction of which orients towards a deficiency in xanthine-oxydase, the increase in which suggests an abnormality in uric acid transport in the proximal tubule (Fanconi syndrome, primary hereditary anomaly of tubular uric acid transport). Hypouricemia does not appear to expose the patient to any danger, but the onset of nephrolithiasis or acute renal failure secondary to the combination of severe hypouricemia and oxidant stress is always possible.
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PMID:[Hypouricemia, an old subject and new concepts]. 1523 14

The frequency of hypercalciuria is increasing in western countries with an incidence of nephrolithiasis which can reach 13%. Hypercalciuria appears as an alteration of the calcium transport system (kidney, bowel, bone) which is regulated by calcitriol and parathormone. The aim of this review was to screen etiologies of hypercalciuria taking into account recent genetic advances (calcium epithelial channel and calcium sensing receptor). Hypercalciuria may be favored by nutritional causes (diet rich in calcium, sodium, carbohydrates, proteins, poor in phosphates and potassium). It may also be related to an increase in calcium absorption (vitamin D excess, primary hyperparathyroidism, sarcoidosis, lymphoma, estrogens, and certain genetic causes), an increase in osteoresorption (bone metastasis, myeloma, Paget, hyperthyroidism, immobilization, hypercortisolism and corticosteroid therapy), or a decrease of kidney tubular resorption (diuretics, Cacci and Ricci, acromegally, Bartter, familial dominant hypocalcemia, Fanconi, Dent, familial hypomagnesemia-hypercalciuria syndrome, type 1 distal tubular acidosis, pseudohypoaldosteronism, diabetes). If no cause is identified, persistence of hypercalciuria after instituting a correct diet is defined as idiopathic hypercalciuria. Treatment of the cause is essential in secondary hypercalciuria, in addition to diet (low sodium intake, normocalcic diet, hydration), associated with thiazide diuretics and biphosphonates if necessary.
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PMID:[Hypercalciuria]. 1635 16


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