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Objective: Renal involvement is a common manifestation of systemic amyloidosis. Amyloid load can be predicted by histopathological grading of amyloid deposits in renal biopsy specimens. This study aimed to determine the relationship of renal amyloid deposition grade with clinical manifestations and outcomes in patients with biopsy-proven renal non-AA amyloidosis. Methods: This retrospective cohort study included 74 subjects with renal non-AA amyloidosis (52 light chain amyloidosis and 22 unclassified amyloidosis). Baseline characteristics and follow-up data were recorded. Pattern and quantity of amyloid deposition in glomeruli, interstitium, vessels, and tubulointerstitial changes were scored. Renal Amyloid Prognostic Score was obtained by addition of all scores and divided into 3 grades (Renal Amyloid Prognostic Score grades I, II, III). Results: In light chain amyloidosis group, the median follow-up was 11 (4-45) months. The baseline estimated glomerular filtration rate was significantly lower among patients with Renal Amyloid Prognostic Score grade III. Death-censored Renal survival was significantly lower among patients with Renal Amyloid Prognostic Score grade III. Renal Amyloid Prognostic Score grade III was a significant predictor of lower renal survival. Patient survival was not significantly different according to Renal Amyloid Prognostic Score grade. Receiving autologous stem cell transplantation treatment was associated with better patient survival. The type of amyloid could not be determined in 22 patients. In this group, baseline estimated glomerular filtration rate was significantly lower in patients with Renal Amyloid Prognostic Score grade III. Conclusions: In patients with light chain amyloidosis, baseline renal function is associated with Renal Amyloid Prognostic Score grade. Renal survival is significantly lower in patients with the highest Renal Amyloid Prognostic Score grade. However, patient survival is not significantly different according to Renal Amyloid Prognostic Score grade. [ABSTRACT FROM AUTHOR]

Objective: Chronic kidney disease is common, irreversible, and associated with high mortality and morbidity. In this study, we aimed to investigate the effects of calcitriol and paricalcitol on chronic kidney disease progression in an adenine induced uremic rat model. Methods: Male Wistar-albino rats were fed a diet containing 0.75% adenine + 1.2% phosphorus for 3 weeks to induce chronic kidney disease. The rats were randomly divided into 6 groups: control group (n = 12), chronic kidney disease group (n = 12), chronic kidney disease+ calcitriol group (n = 12), chronic kidney disease +paricalcitol group (n = 12), calcitriol group (n = 6), paricalcitol group (n = 6). Animals were monitored for weight and systolic blood pressure. The kidney function parameters, parathyroid hormone, monocyte chemoattractant protein-1, and kidney histology were investigated. This research was supported by the Scientific Research Projects Unit (11-TIP-062). Results: Kidney histology proved that the adenine-induced uremic rat model was successfully established. Serum urea, creatinine, and phosphorus were significantly higher in chronic kidney disease, chronic kidney disease + calcitriol, chronic kidney disease +paricalcitol groups compared with the control group (P < .05). Calcitriol and paricalcitol provide effective parathyroid hormone suppression and decrease serum monocyte chemoattractant protein-1 levels in uremic rats. All uremic rats, including the paricalcitol and calcitriol treatment groups, lost weight. Paricalcitol significantly lowered systolic blood pressure in uremic rats (P = .006). Serum calcium was higher in calcitriol group compared with chronic kidney disease group. Paricalcitol caused less hyperphosphatemia in non-uremic rats than calcitriol. Conclusion: Paricalcitol and calcitriol therapy may prevent chronic kidney disease progression in uremic rats as they restore vitamin D metabolism during the disease. [ABSTRACT FROM AUTHOR]

Objective: Urotensin-II is a potent vasoconstrictor peptide and has fibrotic effects in the heart and kidneys and palosuran is a selective urotensin-II receptor antagonist. This study aimed to investigate the effects of palosuran, which has antifibrotic effects, in an acute kidney injury model formed with gentamicin and to reveal new treatment options for acute kidney injury cases. Methods: A total of 24 Wistar albino rats were randomly divided into 3 groups of 8 animals as the control group, the gentamicin group, and the gentamicin+palosuran group. The rats in the control group received a 1 × 1 mL intramuscular injection of saline for 8 days. To create acute kidney injury in the rats in the gentamicin group, an intramuscular injection of 100 mg/kg/day gentamycine was applied for 8 days. In the gentamicin+palosuran group, an intramuscular injection of 100 mg/kg/day gentamycine was applied for 8 days, together with 300 mg/kg palosuran dissolved in distilled water and administered by oral gavage twice a day for the same period. Serum urea, creatinine, calcium, albumin, total protein levels, and urine gamma-glutamyl transferase and protein levels were evaluated for all the groups. In addition, tubular degeneration, tubular necrosis, tubular regeneration, tubulointerstitial nephritis, microcalcification, and total histological scores of these groups were also examined histopathologically. Results: The urine gamma-glutamyl transferase levels of the gentamicin and gentamicin+palosuran groups were significantly higher than those of the control group (311 ± 60.5 and 140 ± 39.5 vs. 0.33 ± 0.22, P < .05). On the eighth day, the gamma-glutamyl transferase levels of the gentamicin+palosuran group were significantly lower than the gentamicin group (311 ± 60.5 vs. 140 ± 39.5, P < .05). A significant decrease was obtained in tubular necrosis in the gentamicin+palosuran group compared to the gentamicin group (2.5 ± 0.3 vs. 1.3 ± 0.4, P< .05). A statistically significant decrease was determined in the total histological score in the gentamicin+palosuran group compared to the gentamicin group (6.4 ± 0.7 vs. 4.7 ± 0.7, P < .05). Our results showed that the urotensin-II receptor antagonist, palosuran, had positive effects on tubular necrosis, tubular degeneration, tubular regeneration, and the total histological score in an experimental acute kidney injury model formed with gentamicin. Conclusion: The study results suggest that urotensin-II may play a role in the physiopathology of acute renal failure associated with gentamicin. These results are promising for the use of palosuran in the treatment of acute kidney injury. [ABSTRACT FROM AUTHOR]