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The current Kidney Disease Outcomes Quality Initiative (KDOQI) staging system of chronic kidney disease (CKD) is simple but too rigid to accommodate variations in renal function observed in the general population. The formula most commonly used to estimate renal function is not validated in subjects without a priori evidence of renal disease. Their combined use results in inappropriate diagnosis of CKD and improbable estimates of prevalence rates. Although this initiative has raised the profile of kidney disease, the exaggeration of the scope of the problem could distract nephrologists from their specialist role. The nephrology community needs a revised staging system for CKD that allows accurate, effective, and timely communication with patients, primary care doctors, public health physicians, and policy makers. Its single most important function will be to identify those patients who will benefit from targeted screening and effective and safe interventions. We offer for discussion a modified definition and staging system of CKD based on the presence of unequivocal, irreversible structural kidney disease, the presence or degree of impairment of kidney function, and the consequences thereof.

In a multicenter, blinded end-point, open-label trial, adults undergoing maintenance hemodialysis were assigned to receive high-dose iron proactively or low-dose iron reactively. High-dose iron therapy was noninferior and led to lower doses of erythropoiesis-stimulating agent.

Patients with autosomal dominant polycystic kidney disease (ADPKD) are at risk of developing intracranial aneurysms, and subarachnoid haemorrhage is a major cause of death and disability. Familial clustering of intracranial aneurysms suggests that genetic factors are important in the aetiology. We tested whether the germline mutation predisposes to this vascular phenotype. DNA samples from patients with ADPKD and vascular complications were screened for mutations throughout the PKD1 and PKD2 genes. Comparisons were made between the pkd1 and pkd2 populations and with a control PKD1 cohort (without the vascular phenotype). Mutations were characterised in 58 ADPKD families with vascular complications; 51 were PKD1 (88%) and seven PKD2 (12%). The median position of the PKD1 mutation was significantly further 5′ in the vascular population than in the 87 control pedigrees (aminoacid position 2163 vs 2773, p=0·0034). Subsets of the vascular population with aneurysmal rupture, early rupture, or families with more than one vascular case had median mutation locations further 5′ (aminoacid position 1811, p=0·0018; 1671, p=0·0052; and 1587, p=0·0003). Patients with PKD2, as well as those with PKD1, are at risk of intracranial aneurysm. The position of the mutation in PKD1 is predictive for development of intracranial aneurysms (5′ mutations are more commonly associated with vascular disease) and is therefore of prognostic importance. Since the PKD1 phenotype is associated with mutation position, the disease is not simply due to loss of all disease allele products.

A complete mutation screen of the ADPKD genes by DHPLC. Genetic analysis is a useful diagnostic tool in autosomal dominant polycystic kidney disease (ADPKD), especially when imaging results are equivocal. However, molecular diagnostics by direct mutation screening has proved difficult in this disorder due to genetic and allelic heterogeneity and complexity of the major locus, PKD1. A protocol was developed to specifically amplify the exons of PKD1 and PKD2 from genomic DNA as 150 to 450bp amplicons. These fragments were analyzed by the technique of denaturing high-performance liquid chromatography (DHPLC) using a Wave Fragment Analysis System (Transgenomics) to detect base-pair changes throughout both genes. DHPLC-detected changes were characterized by sequencing. Cost effective and sensitive mutation screening of the entire coding regions of PKD1 and PKD2 by DHPLC was optimized. All base-pair mutations to these genes that we previously characterized were detected as an altered DHPLC profile. To assess this method for routine diagnostic use, samples from a cohort of 45 genetically uncharacterized ADPKD patients were analyzed. Twenty-nine definite mutations were detected, 26 PKD1, 3 PKD2 and a further five possible missense mutations were characterized leading to a maximal detection rate of 76%. A high level of polymorphism of PKD1 also was detected, with 71 different changes defined. The reproducibility of the DHPLC profile enabled the recognition of many common polymorphisms without the necessity for re-sequencing. DHPLC has been demonstrated to be an efficient and effective means for gene-based molecular diagnosis of ADPKD. Differentiating missense mutations and polymorphisms remains a challenge, but family-based segregation analysis is helpful.

Lithium nephropathy usually develops after 10-20 years of lithium therapy2 and can progress to end-stage renal disease.3,4 A renal biopsy that shows chronic tubulointerstitial nephritis, tubular dilatation and atrophy, interstitial fibrosis, cortical and medullary cyst formation, and focal segmental glomerulosclerosis, supports a diagnosis of lithium nephropathy.2-5 MRI is a less invasive method for diagnosing chronic lithium nephropathy, and is particularly useful in situations when a renal biopsy might not be feasible or appropriate.5 MRI images show a characteristic pattern of symmetrical and uniform corticomedullary microcysts (usually <2 mm) in both kidneys.4,5 MRI is superior to other imaging modalities,4,5 but if microcysts are sparse, or numerous but predominantly localised to the cortex, MRI is less specific.

The average glomerular filtration rate (GFR) is lower in the elderly than in the young and is usually a consequence of biological ageing, the rate of which varies between individuals. In some subjects, the decline is aggravated by concomitant vascular disease. The prevalence of significant kidney disease in the elderly has been overestimated - largely by rendering a diagnosis of chronic kidney disease by reference to estimates of GFR which are found in the young. A stable low GFR in the elderly, provided it is physiologically sufficient to meet homeostatic demands, is not a disease per se and seldom progresses to true kidney failure. However, it can be a risk factor for acute kidney injury drug misdosing, and possibly cardiovascular disease, so it should be noted. Copyright © 2011 S. Karger AG, Basel [PUBLICATION ABSTRACT]

Background/Aims: Adult polycystic kidney disease (ADPKD) has a predictable natural history and the relative lack of co-morbidity allows a relatively unconfounded assessment of survival. We examined whether survival on renal replacement treatment (RRT) has improved over the last four decades compared to that in the general population. Methods: We conducted a retrospective cohort study of all patients with ADPKD who received RRT between 1971 and 2000 at the Oxford Kidney Unit. The main exposure was period of start of treatment (1971-1985 vs. 1986-2000) and the key outcome was overall survival. Standard Cox regression techniques were used to assess the association between these baseline variables and survival. Results: Age at start of RRT (HR per 1 year 1.08; 95% CI 1.06-1.10) and presence of a functioning transplant (HR 0.22; 95% CI 0.16-0.31) were associated with improved survival in unadjusted analyses. After adjustment for age the period of treatment also became a significant predictor of overall survival (HR 0.67; 95% CI 0.47-0.97). Conclusions: Survival on RRT appears to have improved and exceeds that observed in the general population, such that RRT now provides almost two-thirds of the life expectancy of the general population, compared to about half in earlier decades. Copyright © 2011 S. Karger AG, Basel [PUBLICATION ABSTRACT]

According to the Kidney Disease Outcomes Quality Initiative guidelines, estimated glomerular filtration rate can be used to diagnose chronic kidney disease. The authors of this Viewpoint argue, however, that reliance on estimated glomerular filtration rates alone encourages an erroneous disregard of age, gender and other evidence of kidney disease, such as proteinuria. Consequently, mandatory reporting of estimated glomerular filtration rate leads to misdiagnosis of chronic kidney disease and to the unhelpful referral of healthy individuals to nephrologists.