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Abstract Introduction Little is known about the responses of natriuretic peptides to developing congestive heart failure in ‘anephric’ end-stage kidney disease. Case presentation We present three consecutive cases of surgically-induced anephric patients in a critical care environment: a 28-year-old Caucasian woman (with congestive heart failure), a 42-year-old Caucasian woman (without congestive heart failure), and a 23-year-old Caucasian woman (without congestive heart failure). Our limited study data indicate that cut-off values advocated for B-type natriuretic peptide and its N-terminal fragment to ‘rule out’ congestive heart failure in two of our end-stage kidney disease patients (without congestive heart failure) are largely appropriate for anephric patients. However, our index (first) patient developed congestive heart failure accompanied by the phenomenon of massive and persistent elevation of these natriuretic levels. Conclusion Our findings suggest that patients from the anephric subclass suffering from congestive heart failure will develop supramaximal elevation of B-type natriuretic peptide and its N-terminal fragment, implying the need for dramatically higher cut-off values with respective magnitudes of the order of 50-fold (B-type natriuretic peptide ~5780pmol/L; 20,000ng/L) to 100-fold (N-terminal fragment ~11,800pmol/L; 100,000ng/L) higher than current values used to ‘rule in’ congestive heart failure. Further research will be required to delineate those cut-off values. The role of our devised ‘Blood Volume – B-type natriuretic peptide feedback control system’ on ‘anatomical’ and ‘functional’ anephric patients led to significant mathematically-enriched arguments supporting our proposal that this model provides plausible explanations for the study findings, and the model lends support to the important hypothesis that these two groups of anephric patients inflicted with congestive heart failure should effectively have similar natriuretic response behavior.

Goodpasture's disease, also known as antiglomerular basement membrane disease, is a rare but important cause of pulmonary haemorrhage (PH) and rapidly progressive crescentic glomerulonephritis (GN) that leads to irreversible renal failure. As an autoimmune disease, it is characterized by the production of pathogenic autoantibodies to the NC1 domain of the alpha 3 chain of type IV collagen which bind to basement membranes predominantly found in glomeruli and pulmonary tissue. Antiglomerular basement membrane disease usually presents with acute renal failure and PH. In the urine, there is the typical picture of a rapidly progressive GN with red and white cell casts and proteinuria.

Abstract: Objective: To investigate the mechanisms underlying peripheral neuropathy and to provide insights into axonal Na+/K+ pump function in patients with end-stage kidney disease (ESKD). Methods: Nerve excitability was assessed in 10 ESKD patients before and after a single session of haemodialysis and in 29 age-matched control subjects. Changes in excitability were recorded at baseline and following maximal voluntary contraction (MVC) of abductor pollicis brevis (APB) for 60s. Serum concentrations of putative neurotoxins including potassium, urea, parathyroid hormone and beta-2-microglobulin were also measured. Results: Baseline excitability values were consistent with axonal depolarisation prior to dialysis. Following maximal voluntary contraction (MVC), there was an increase in threshold, which was associated with reduced strength-duration time constant and increased superexcitability, consistent with axonal hyperpolarisation. These changes were quantitatively similar for patients and controls, arguing against any significant reduction in the axonal Na+/K+ pump in ESKD. Following dialysis, activity-dependent changes were less in ESKD, which suggests greater Na+/K+ pump activity prior to dialysis, the opposite of the changes expected with reduced Na+/K+ pump function. The reduced post-contraction threshold change in post-dialysis recordings is likely to be secondary to relative hyperpolarisation of the axonal membrane following dialysis and reduction in K+ concentration. Conclusions: Our findings suggest that Na+/K+ pump function is not impaired in patients with ESKD. Significance: Pre-dialysis excitability changes in ESKD patients may be explained on the basis of hyperkalaemia. Alteration in Na+/K+ pump function does not appear to be a contributing factor to the development of neuropathy in ESKD patients. [Copyright &y& Elsevier]