Corticosteroids in Patients with IgA Nephropathy and Severe Chronic Renal Damage

Little is known about the utility of treating patients with advanced IgA nephropathy (IgAN). From 2001 to 2005, four patients came to our observation because of serum creatinine higher than 3 mg/dL, proteinuria ranging from 1.8 to 5.1 g/day, and a histological picture of diffuse sclerotic lesions. A corticosteroid course of 12 months was given. Patients were observed for a mean follow up of 84 months. At the end of the steroid course, proteinuria lowered quickly below 1 g/day in two patients, whereas the other two experienced a slower and less persistent decrease of proteinuria. Despite similar lesion severity at renal biopsy, renal function stabilized only in these two ones. In conclusion, these preliminary observations suggest a possible efficacy of corticosteroids in slowing down the progression of renal disease and in postponing the need of dialysis in IgAN patients with stage IV CKD and severe chronic histological lesions

Effect of oral liposomal iron versus intravenous iron for treatment of iron deficiency anaemia in CKD patients: A randomized trial

IntroductionIron deficiency is a common cause of anaemia in non-dialysis chronic kidney disease (ND-CKD). Controversies exist about the optimal route of administration for iron therapy. Liposomal iron, a new generation oral iron with high gastrointestinal absorption and bioavailability and a low incidence of side effects, seems to be a promising new strategy of iron replacement. Therefore, we conducted a study to determine whether liposomal iron, compared with intravenous (IV) iron, improves anaemia in ND-CKD patients. MethodsIn this randomized, open-label trial, 99 patients with CKD (stage 3-5, not on dialysis) and iron deficiency anaemia [haemoglobin (Hb) ≤12 g/dL, ferritin ≤100 ng/mL, transferrin saturation ≤25%] were assigned (2:1) to receive oral liposomal iron (30 mg/day, Group OS) or a total dose of 1000 mg of IV iron gluconate (125 mg infused weekly) (Group IV) for 3 months. The patients were followed-up for the treatment period and 1 month after drug withdrawal. The primary end point was to evaluate the effects of the two treatments on Hb levels; the iron status, compliance and adverse effects were also evaluated. ResultsThe short-term therapy with IV iron produced a more rapid Hb increase compared with liposomal iron, although the final increase in Hb was similar with either treatment; the difference between the groups was statistically significant at the first month and such difference disappeared at the end of treatment. After iron withdrawal, Hb concentrations remained stable in Group IV, while recovered to baseline in the OS group. The replenishment of iron stores was greater in the IV group. The incidence of adverse event was significantly lower in the oral group (P < 0.001), and the adherence was similar in the two groups. ConclusionsOur study shows that oral liposomal iron is a safe and efficacious alternative to IV iron gluconate to correct anaemia in ND-CKD patients, although its effects on repletion of iron stores and on stability of Hb after drug discontinuation are lower

Data on the assessment of LV mechanics by speckle tracking echocardiography in ADPKD patients

In this article, we report anthropometric, clinical and laboratory data from Autosomal Dominant Polycystic Kidney Disease (ADPKD) patients with mild to moderate renal dysfunction and normal LV ejection fraction and from age- and sex-matched healthy controls and renal controls. Factors influencing LV untwisting rate in the group of ADPKD patients are also reported. For further interpretation and discussion please refer to the research article “Left ventricular dysfunction in ADPKD and effects of Octreotide-LAR: a cross-sectional and longitudinal sub study of the ALADIN trial” (Spinelli et al., 2018) [1]

Nephrotic syndrome and autosomal dominant polycystic kidney disease

BackgroundAutosomal dominant polycystic kidney disease (ADPKD) is an inherited disorder characterized by the development and growth of cysts in the kidneys and other organs. In ADPKD patients, nephrotic range proteinuria is unusual and needs to be investigated further to exclude coexisting glomerular disease. Among the anecdotal case reports of ADPKD associated with nephrotic syndrome, focal segmental glomerulosclerosis occurs most frequently.MethodsWe report the case of a 26-year-old male with ADPKD and concomitant nephrotic syndrome, in which an ultrasound (US)-guided renal biopsy showed a mesangioproliferative glomerulonephritis. We treated the patient with prednisone 1 mg/kg/day, because of the failure of treatment with angiotensin-converting enzyme inhibitor/angiotensin receptor blocker association.ResultsAfter 6 months of steroid treatment, we observed a stability of his GFR and a reduction of proteinuria.ConclusionThis case report and other cases of the literature underline the importance of a renal biopsy in patients with ADPKD and nephrotic syndrome in order to make an accurate diagnosis and an appropriate treatment/prevention of renal function deterioration. © 2012 The Author

Renal survival.

<p>(A) Kaplan-Meier estimates of proportion of renal survival (absence of creatinine doubling) in the 325 patients by TAp groups. Estimated 5-year overall survival rates were 97.7% (95% CI 84.9–99.7) for patients with <0.3 g/day; 95.1% (95% CI 89.4–97.8) for patients with 0.3–0.9 g/day, 92.1% (95% CI 79.8–96.3) for those with 1–1.9 g/day, 69.4% (95% CI 46.3–84.1) for those with 2–2.9 g/day and 29.0% (95% CI 14.6–45.1) for those with ≥3 g/day. (B) Kaplan-Meier estimates of proportion of renal survival (absence of ESRD) in the 325 patients by TAp groups. Estimated 5-year overall survival rates were 100% (95% CI: not calculable) for patients with <0.3 g/day; 96.5% (95% CI 90.1–98.7) for patients with <0.3–0.9 g/day, 95.6% (95% CI 84.3–99.2) for those with 1–1.9 g/day, 69.1% (95% CI 45.6–84.0) for those with 2–2.9 g/day and 46.9% (95% CI 27.7–63.9–45.1) for those with ≥3 g/day.</p

Characteristics of the three considered trials.

<p>Characteristics of the three considered trials.</p

Change in eGFR during FU according to TAp in all patients and in patients with eGFR <30 ml/min.

<p>Change in eGFR during FU according to TAp in all patients and in patients with eGFR <30 ml/min.</p