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PubMed1984

The intrarenal distribution of aztreonam in healthy and diseased kidneys: clinical therapeutic implications.

Using a healthy canine model, we evaluated the influence of renal physiological activity on the stability, intrarenal distribution, and clearance of aztreonam and compared the results with the concentrations of aztreonam that can be achieved in the scarred devitalized renal tissues of patients with end-stage kidney disease. Renal physiological activity significantly modulates the intrarenal distribution of aztreonam. During the production of maximally acid-concentrated urine, urinary aztreonam levels, clearance rates, and inner zone renal tissue concentrations are increased. Aztreonam concentrations in the parenchyma of severely diseased kidneys are significantly reduced in comparison with healthy tissues; nonetheless, the values are similar to concurrent serum drug levels, a result suggesting that treatment may provide adequate coverage for aztreonam-susceptible organisms.

Animals↗
PubMed1971

Disproportionate inhibition of sodium reabsorption in the unilaterally diseased kidney of dog and man after an acute saline load.

Clearance studies were performed on 49 split-bladder dogs with a unilateral pyelonephritic or remnant kidney and three patients with unilateral kidney disease to examine the effects of an acute saline load on the diseased kidney (DK) as opposed to a simultaneously studied, contralateral control kidney (CK), which also served to maintain a nonuremic environment. Before saline loading, base line studies in many of the dogs and the three humans were in agreement with previously published data. However, in dogs with a severe pyelonephritic lesion, a greater difference in DK vs. CK fractional excretion of sodium (FE(Na)) and water was noted, whose magnitude was inversely correlated with the level of glomerular filtration rate (GFR) and maximum urine osmolality of DK compared to CK. An acute saline load (75 ml/kg) resulted in an inhibition of fractional sodium and water reabsorption in the diseased dog kidney which was disproportionately greater than in the simultaneously studied CK, regardless of the type or severity of the lesion. While mean DK GFR for all dogs increased 15% more than CK GFR, failure of FE(Na) to increase after induction of a disproportionate increase in DK GFR with parathyroid hormone suggested that the saline-induced disproportionate increase in GFR was not solely responsible for the exaggerated inhibition of fractional sodium and water reabsorption in the diseased dog kidney. Studies in the three patients after saline loading (25 ml/kg) revealed a similar disproportionate resetting of glomerulotubular balance.Thus, regardless of base line function before expansion, the unilaterally diseased kidney of dog and man possesses unique characteristics in the absence of uremia which render it more reactive to the stimuli produced by acute saline loading. This suggests that the intrarenal environment of the kidney with a reduced nephron population may under some circumstances serve as a determinant of its function.

Acetazolamide↗
PubMed1989

[Acquired cystic kidney disease and autosomal dominant polycystic kidney disease--precancerous condition?].

Acquired cystic kidney disease (ACKD) is a frequent complication of end-stage renal disease. In about 50% of patients on chronic haemodialysis treatment, secondary cysts are detected by sonography/computed tomography or at autopsy. ACKD is associated with an increased risk for the development of renal neoplasias. Renal adenomas are found in 8.8% of the cases, renal cell carcinomas are observed in 2.9% of the patients. The prevalence of renal cell carcinoma is 5-10 times greater in ACKD than in the general population. Therefore, ACKD should be considered as a precancerous condition carrying an increased risk for the development of renal cell carcinoma. Consequently patients with ACKD need careful and regular clinical observation and monitoring by ultrasound or computed tomography. An increased risk for the development of renal cell carcinoma has also been discussed in autosomal dominant polycystic kidney disease (ADPKD) based on anecdotal observations. A careful analysis of the literature as well as a retrospective examination of 86 necropsies (1951-1985) and 25 nephrectomy specimens with ADPKD revealed only one patient with renal cell carcinoma. With respect to the incidence of renal cell carcinoma and the frequency of ADPKD (1:1000) in the general population, the present data do not permit the conclusion that ADPKD represents a precancerous condition.

Genes, Dominant↗
PubMedDate not supplied

Clinical epidemiology of cardiovascular disease in chronic kidney disease prior to dialysis.

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Both in dialysis and in transplant patients, CVD remains the leading cause of death. There is accumulating evidence that the increase in CVD burden is present in patients prior to dialysis, due to both conventional risk factors as well as those specific to kidney disease. Of importance is that even in patients with mild kidney disease, the risk of cardiovascular events and death is increased relative to patients without evidence of kidney disease. The new classification system proposed by the National Kidney Foundation as part of the Dialysis Outcomes Quality Initiative (DOQI) process describes the five stages of kidney disease, as well as those complications associated with chronic kidney disease (CKD), in particular cardiovascular risk factors and disease. Patients with kidney disease are deemed to be at highest cardiovascular risk. CVD, defined as the presence of either congestive heart failure (CHF), ischemic heart disease (IHD), or left ventricular hypertrophy (LVH), is prevalent in cohorts with established CKD (8-40%). The prevalence of hypertension, a major risk factor for coronary artery disease (CAD) and LVH is high in patients with CKD (87-90%). At least 35% of patients with CKD have evidence of an ischemic event (myocardial infarction or angina) at the time of presentation to a nephrologist. The prevalence of LVH increases at each stage of CKD, reaching 75% at the time of dialysis initiation, and the modifiable risk factors for LVH include anemia and systolic blood pressure, which are also worse at each stage of kidney disease. Even under the care of nephrologists, a change in cardiac status (worsening of heart failure or anginal symptoms) occurs in 20% of patients. The presence of CVD predicts a faster decline of kidney function and the need for dialysis, after controlling for all other factors including glomerular filtration rate (GFR), age, and the presence of LVH. This article describes the new classification system for staging of CKD, defines and describes CVD in CKD, and reviews the evidence and its limitations with respect to the current understanding of CKD and CVD. Specifically, methodologic issues related to survival and referral bias limit our current understanding of the complex interaction of conventional and nonconventional kidney disease-specific risk factors. We identify the importance of well-conducted studies of patient groups with and without CVD, with and without CKD, in order to better understand the complex physiology so that treatment strategies can be appropriately applied.

Cardiovascular Diseases↗
PubMed2007

TRP channels and kidney disease: lessons from polycystic kidney disease.

Important insights in to the function of members of the TRP (transient receptor potential) channel superfamily have been gained from the identification of disease-related mutations. In particular the identification of mutations in the PKD2 gene in autosomal dominant polycystic kidney disease has revealed a link between TRP channel function, mechanosensation and the role of the primary cilium in renal cyst formation. The PKD2 gene encodes TRPP2 (transient receptor potential polycystin 2) that has significant homology to voltage-activated calcium and sodium TRP channels. It interacts with polycystin-1 to form a large membrane-associated complex that is localized to the renal primary cilium. Functional characterization of this polycystin complex reveals that it can respond to mechanical stimuli such as flow, resulting in influx of extracellular calcium and release of calcium from intracellular stores. TRPP2 is expressed in the endoplasmic reticulum/sarcoplasmic reticulum where it also regulates intracellular calcium signalling. Therefore TRPP2 modulates many cellular processes via intracellular calcium-dependent signalling pathways.

Amino Acid Sequence↗
PubMed2005

The clinical epidemiology of cardiovascular disease in chronic kidney disease.

PURPOSE OF REVIEW: To review recent publications concerning the epidemiology and management of cardiovascular disease in the stages of chronic kidney disease. RECENT FINDINGS: Chronic kidney disease is a state of increased risk for atherosclerotic and cardiomyopathic disease. The mechanisms of cardiovascular disease probably change with the different stages of chronic kidney disease. Both proteinuria and decreased glomerular filtration rate are probably independent cardiovascular disease risk factors, although the impact of the latter is modest. Traditional risk factors are important predictors of cardiovascular disease in chronic kidney disease. Recent randomized controlled trials and cohort studies have supported interventions for smoking cessation, blood pressure control, renin-angiotensin system blockade, the correction of lipid abnormalities, and utilizing antiplatelet agents. Some uraemia-related risk factors predict the development of cardiovascular disease, particularly hypoalbuminaemia, inflammation, anaemia, and homocysteinaemia. However, randomized controlled trials of anaemia correction and of an increased quantity of dialysis were negative. SUMMARY: The role of oxidant stress, divalent ion abnormalities, various lipid abnormalities and other potential factors require further investigation. To determine whether these uraemia-related factors are markers of cardiovascular disease risk or are actually cardiotoxic requires additional randomized controlled trials.

Atherosclerosis↗
PubMed2005

Prevalence of family history of kidney disease and perception of risk for kidney disease: a population-based study.

BACKGROUND: A family history of kidney disease is associated with an increased risk for end-stage renal disease (ESRD). However, it is unclear whether blacks are more likely to have a family history of ESRD than other groups independently of kidney disease risk factors. Moreover, their risk perception for kidney disease is unknown. METHODS: The association of race with family history of ESRD and perception of risk for kidney disease was examined in a representative random sample of 402 Georgia residents who completed a telephone interview. Logistic regression analysis was used to derive adjusted odds ratios and 95% confidence intervals for the association between race and family history of ESRD, controlling for age, sex, education level, being a Georgia native, diabetes, hypertension, and personal history of kidney disease. A multinomial logit model was used to derive adjusted estimates for the association between race and perception of risk for kidney disease. RESULTS: Mean age was 43.2 years, 41.0% of respondents were men, 20.1% were black, 6.6% had diabetes, 21.4% had hypertension, 1.6% had a personal history of kidney disease, and 3.7% reported a family member with ESRD. Although blacks were more likely to report a family history of ESRD (odds ratio, 6.43; 95% confidence interval, 2.02 to 20.43), their perception of risk was not greater. CONCLUSION: Although blacks are approximately 6 times as likely to report a family history of ESRD independently of a personal history of kidney disease, diabetes, or hypertension, they do not perceive themselves as more vulnerable for kidney disease.

Adult↗
PubMed2005

Asymmetric dimethylarginine and progression of chronic kidney disease: the mild to moderate kidney disease study.

Reduced bioavailability of nitric oxide (NO) is thought to play an important role in progression of renal damage. The hypothesis that the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) is involved in progression of kidney disease was tested. Plasma ADMA concentrations and other putative progression factors were assessed in 227 relatively young patients (45.7 +/- 12.6 yr) with nondiabetic kidney diseases and mild to moderate renal failure. Progression assessed as doubling of serum creatinine and/or renal replacement therapy was evaluated prospectively. Baseline plasma ADMA concentrations in renal patients correlated significantly with serum creatinine (r = 0.595), GFR (r = -0.591), age (r = 0.281), and proteinuria (r = 0.184; all P < 0.01). Patients who reached an end point during follow-up were significantly older (P < 0.05) and had significantly higher creatinine, ADMA, and parathyroid hormone blood concentrations and protein excretion rates at baseline, whereas GFR and hemoglobin were significantly lower (all P < 0.01). Cox regression analysis revealed baseline serum creatinine (odds ratio 2.00; 95% confidence interval [CI] 1.61 to 2.49; P < 0.001) and ADMA (odds ratio 1.47; 95% CI 1.12 to 1.93 for an increment of 0.1 mumol/L; P < 0.006) as independent predictors of disease progression. In patients with ADMA levels above median, progression was significantly faster (P < 0.0001), and their mean follow-up time to a progression end point was 52.8 mo (95% CI 46.9 to 58.8) as compared with 71.6 mo (95% CI 66.2 to 76.9) in patients with ADMA levels below the median. The endogenous NO synthase inhibitor ADMA is significantly associated with progression of nondiabetic kidney diseases. Lowering plasma ADMA concentrations may be a novel therapeutic target to prevent progressive renal impairment.

Adult↗
PubMed2005

Apolipoprotein A-IV predicts progression of chronic kidney disease: the mild to moderate kidney disease study.

It has not been established firmly whether dyslipidemia contributes independently to the progression of kidney disease. Lipid and lipoprotein parameters, including levels of total, HDL, and LDL cholesterol; triglycerides; lipoprotein(a); apolipoprotein A-IV; and the apolipoprotein E and A-IV polymorphisms, were assessed in 177 patients who had mostly mild to moderate renal insufficiency and were followed prospectively for up to 7 yr. Progression of kidney disease was defined as doubling of baseline serum creatinine and/or terminal renal failure necessitating renal replacement therapy. In univariate analysis, patients who reached a progression end point (n = 65) were significantly older and had higher serum creatinine and proteinuria as well as lower GFR and hemoglobin levels. In addition, baseline apolipoprotein A-IV and triglyceride concentrations were higher and HDL cholesterol levels were lower. Multivariate Cox regression analysis revealed that baseline GFR (hazard ratio 0.714; 95% confidence interval [CI] 0.627 to 0.814 for an increment of 10 ml/min per 1.73 m(2); P < 0.0001) and serum apolipoprotein A-IV concentrations (hazard ratio 1.062; 95% CI 1.018 to 1.108 for an increment of 1 mg/dl; P = 0.006) were significant predictors of disease progression. Patients with apolipoprotein A-IV levels above the median had a significantly faster progression (P < 0.0001), and their mean follow-up time to a progression end point was 53.7 mo (95% CI 47.6 to 59.8) as compared with 70.0 mo (95% CI 64.6 to 75.4) in patients with apolipoprotein A-IV levels below the median. For the apolipoprotein E polymorphism, only the genotype epsilon2/epsilon4 was associated with an increased risk for progression. In summary, this prospective study in patients with nondiabetic primary kidney disease demonstrated that apolipoprotein A-IV concentration is a novel independent predictor of progression.

Adult↗