Iranian Journal of Kidney Diseases
Volume:16 Issue: 2, Mar 2022

Zinc is the second most abundant essential trace element in the human body with important regulatory functions in cellular and subcellular levels in several tissues. Zinc deficiency is associated with the development and progression of chronic kidney disease (CKD) and its complications. With the progression of CKD to end-stage kidney disease (ESKD) and initiation of dialysis, zinc is further removed from the body, potentiating the zinc deficiency. Dietary intake plays a major role in zinc-deficiency-related risks and progression of CKD. By taking into account the evidence from clinical studies depicting the mutual correlations between zinc and CKD, and the plausibility based on animal studies, it can be deduced that zinc deficiency has a causative role in CKD and its progression. This review highlights the role of zinc deficiency in kidney disease and the possible indication for supplementation of zinc at various stages of CKD.

Cardiovascular disease (CVD) may accompany chronic kidney disease (CKD), resulting in additional complications and increased death rate. This study was performed to evaluate cardiac structure and function and several risk factors in hospitalized CKD children.

Seventy-four children with CKD were enrolled in this cross-sectional descriptive study. Two-dimensional and M-mode ultrasonography, Doppler flow velocity and Tissue Doppler Imaging (TDI) were used to evaluate cardiac chamber size, left ventricular mass (LVM) and echocardiographic indices of ventricular function.

Advanced stages of CKD showed statistically insignificant increased LVM and LVM indexed to height2.7 (LVMI), and mildly reduced diastolic function. Hypertensive patients had an insignificant increase in the incidence of left ventricular hypertrophy (LVH) defined as LVMI greater than 95th percentile for age and sex and LVH2 as LVMI2 more than 95 gr/m2 for girls and more than 115gr/ m2 for boys older than 8 years. Patients with LVH had lower left ventricular ejection fraction (LVEF) and abnormal right ventricular (RV) function based on the tricuspid valve systolic velocity (TV S′) survey. LVH2 cases, however, revealed decreased LV systolic function according to ejection fraction (EF) and abnormal mitral valve systolic velocity (MV S′).

LVH related to hypertension and mild systolic and diastolic dysfunction were more prevalent in advanced CKD cases, however TDI showed no statistically significant difference in the prevalence of MV S′ and TV S′. We recommend strict blood pressure control and prevention of renal function deterioration as effective tools for cardiac protection in CKD children.

Introduction. The antioxidant activity of curcumin (CMN) has been evaluated in several studies. We aimed to examine the protective effect of curcumin on gentamicin-induced nephrotoxicity in rats, both at histological and immunohistochemical levels. Methods. Forty male Wistar albino rats were assigned into four groups of 10 as follows: group 1: control, group 2: curcumin for 15 days, group 3: gentamicin for the last 10 days, and group 4: curcumin for 15 days and gentamicin for the last 10 days. Curcumin (100 mg/kg/d) was gavaged, and gentamicin (80 mg/kg/d) was injected intraperitoneally. Kidney tissues and blood were collected for histological, immunohistochemical and biochemical studies. Body weight and kidney weight/body weight changes were recorded. Results. Gentamicin nephrotoxicity was characterized by a significant rise in serum urea and creatinine levels and a significant reduction in body weight and an increase in kidney weight/body weight. The gentamicin group showed degenerative changes in tubules and glomeruli together with, increased phosphorylated (p)-p38 mitogen-activated protein kinase (p38 MAPK) positive cells in immunohistochemical evaluation, increased immunoreactivity of nuclear factor-kappa B (NFkB), and decreased immunoreactivity of nuclear factor erythroid 2-related factor 2 (Nrf2). Curcumin diminished body weight loss caused by gentamicin administration but, did not change the kidney weight/body weight. Moreover, curcumin ameliorated the histological alterations and reduced the biochemical parameters. Additionaly, curcumin significantly decreased p-p38 MAPK positive cells and NFkB immunoreactivity, while significantly increasing Nrf2 immunoreactivity in the kidney tissue. Conclusion. We conclude that curcumin may attenuate gentamicininduced nephrotoxicity by supprresing the p38 MAPK and NFkB, and activating the Nrf2 signaling pathways.

Geranium has various antioxidant, anti-inflammatory, and anti-microbial effects. Prescribing glutathione probably enhances the protective mechanisms of nephrons against oxidative stresses. This study aimed to evaluate the protective effect of geranium on acetaminophen-induced nephrotoxic rats.

In the present study, 70 mice were divided into seven groups. In five groups (T1, T2, T3, T4, and T5), different doses of geranium were given by gavage to the mice for seven days, then on the 8th day, a high dose of acetaminophen was administered intraperitoneally. Group T5 only received geranium extract. The control group received neither acetaminophen nor the extract while the last group received only a toxic dose of acetaminophen. Twenty-four hours after the last drug administration, blood samples were taken to check the levels of uric acid, blood nitrogen, and creatinine. The data were analyzed in SPSS version 25. To investigate the between-group factors’ effects, one-way ANOVA with Tukey’s post hoc test was performed at the alpha level of < 0.05.

The differences between the levels of blood creatinine, urea, and uric acid were significant (P < .001) among the groups. The mean blood urea for groups T3 and T4 were similar, and they had a significant difference in comparison with the control group (P < .05). The mean creatinine levels were similar between T4, T5, and the control groups and were significantly different from the other groups (P < .05). Blood uric acid for groups T1 and T2 were similar to Group B and higher than the other groups (P < .05).

The results showed that by strengthening cell protection mechanisms against oxidative stress, geranium extract reduces the toxic effects of acetaminophen on mice’s kidney function and thus ameliorates the damage. As a result, the geranium extract has no adverse effects on kidney function.

Crescents (C) have been recently added to the Oxford classification of IgA nephropathy (IgAN) consisting of mesangial hypercellularity (M), endocapillary hypercellularity (E), segmental sclerosis (S) and tubular atrophy/ interstitial fibrosis (T) (MEST). The aim of the study was to assess the added impact of crescents, on development of end-stage kidney disease (ESKD) in IgAN patients .

On-hundred fifteen IgAN patients (76% male, mean age: 37 ± 13 years, mean serum creatinine: 4.0 ± 4.3 mg/dL, mean proteinuria: 3.4 ± 2.5 g/d) were followed for 43 ± 29 months. MEST score was defined according to Oxford classification (M0/M1, E0/ E1, S0/S1). To increase the power, T was defined as T0 ≤ 25% and T1 > 25%. Crescents were defined as C0, “absence” and C1 “at least one” crescent. In sensitivity analysis, the risk of ESKD was estimated at different cut-off levels of at least 10, 20, and 30% crescents.

Forty patients (35%) developed ESKD. Among those 14% with at least one crescent, 21 patients (46%) developed ESKD. In 11 patients with C ≥ 30%, 66% and among 57 patients with T1, 60% and in 27 patients with T1 + C1 74% developed ESKD. In adjusted model, only C ≥ 30% (HR = 3.15, 95% CI: 1.15 to 11.00; P = 0.027) and the presence of T1+ C1 (HR = 7.18, 95% CI: 1.90 to 27.10, P = 0.004) were associated with increased risk of ESKD. The median kidney survival was 78.0 months (95% CI: 70.5 to 85.6 months), in patients with T0 + C0 and 32.3 months (95% CI: 19.3 to 45.3 months) in patients with T1 + C1.

In this study T ≥ 25%, and the presence of crescents ≥ 30%, were independently associated with increased risk of ESKD. This risk was strongly increased in the combined presence of at least one crescent and T1 ≥ 25%, that predicted a high ESKD rate.

The significant role of oxidative stress in the occurrence and development of a variety of diseases, including renal ischemia-reperfusion injury, has been thoroughly studied in this research. In this study, the protective role of indole-acetic acid on antioxidant, apoptotic and histopathological parameters in a rat model of renal ischemia-reperfusion (IR) injury were investigated.

We divided 40 rats into the following four groups (n = 10 per group): healthy control, IR control, IR + indole-acetic acid 40 mg/kg, and IR + indole-acetic acid 60 mg/kg. After two weeks, the rats were anesthetized and their kidneys were removed. The effects of indole-acetic acid on biochemical parameters [glutathione peroxidase (GPx) and catalase (CAT) were measured by spectrophotometry and expression of apoptotic genes (BAX and Bcl2) using real-time RT-PCR. Tubular necrosis was evaluated using a histopathological study.

There were significant improvements in biochemical parameters (GPx), expression of the apoptotic genes (BAX) and tubular necrosis in rats treated with indole-acetic acid.

Indole-acetic acid could reduce the effects of factors involved in the pathogenesis of IR, including oxidative stress, apoptosis and tubular necrosis. It can be recommended that, indoleacetic acid may be useful for amelioration of damages caused by IR.

Secondary hyperparathyroidism may cause an increase in blood pressure among maintenance hemodialysis (MHD) patients. The objective of this study were to observe the effects of different treatment modalities of hyperparathyroidism on blood pressure among MHD patients with secondary hyperparathyroidism.

This retrospective cohort study was conducted on 69 patients divided into three groups, based on the therapeutic strategies (parathyroidectomy, n = 22; cinacalcet, n = 14; calcitriol, n = 33). Changes in systolic blood pressure (SBP) and diastolic blood pressure (DBP) from pre- to post-treatment visits at 1st, 3rd, 6th, and 12th month were analyzed by mixed-effects repeated-measures model. Serum levels of the renin-angiotensin system (RAS) mediators (renin and aldosterone), endothelin, and echocardiography were compared before and after one year of treatment within the three groups.

Changes in blood pressure were significantly different among the three groups (SBP: P for group < 0.05; DBP: P for group < .05; both P for group × time interaction < .05). SBP and DBP showed a significant downward trend in the surgery group (P for change in SBP < .05, P for change in DBP < .001, adjusted mean change of SBP = -12.16 (-19.70 to -4.62) mmHg and of DBP = -6.82 (-10.58 to -3.06) mmHg in the surgery group on the 12th month). Diastolic BP showed a significant upward trend in the cinacalcet group (P for change in DBP < .05, adjusted mean change of DBP = 6.03 (2.08 to 9.98) mmHg in cinacalcet group in the 12th month). No significant change in BP was observed in the calcitriol group. The levels of serum RAS mediators, endothelin, or cardiac ultrasonography didn’t change and almost remained consistent during the treatment course.

Blood pressure decreased significantly over a year in patients with parathyroidectomy, while DBP increased significantly over time by cinacalcet treatment.

Acute kidney injury (AKI) , proteinuria in the nephrotic or subnephrotic range and hematuria might be seen in patients with coronavirus disease 2019 (COVID-19) infection. In this case study we present a 59 years old manwho was diagnosed with immune-complex glomerulonephritis after development of rapidly progressive kidney failure accompanied by pulmonary hemorrhage, 2 months after COVID-19 infection. The patient was hospitalised with the diagnosis of acute kidney injury and nephrotic syndrome. Hemodialysis was performed due to uremic symptoms. Cyclophosphamide, methylprednisolone and plasmapheresis were started. Pathologic examination of kidney biopsy revealed features compatible with immune complex-related acute glomerulonephritis. Cyclophosphamide and plasmapheresis were discontinued , and treatment with 1 mg/kg/day methylprednisolone was continued. Immune-complex glomerulonephritis can be seen following COVID-19 infection. İt is important to diagnose this disease entity as soon as possible . Steroidtherapy and other supportive modalities might be sufficient in the treatment.