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Introduction: The aims of this study were to assess the renal expression of angiotensin II type 1 receptor (AT1R), angiotensin II type 2 receptor (AT2R), and MAS receptor in human type 2 diabetic nephropathy (DN).Materials and Methods: In total, 115 patients diagnosed with DN by renal biopsy were enrolled in this study. The protein expression levels of the AT1R, AT2R, and MAS receptors were assessed by immunohistochemistry.Results: The protein expression levels of AT1R, AT2R, and MAS receptor in the renal biopsy tissue were correlated with the pathologic classification of DN. Tubulointerstitial AT1R expression in patients of class IIb was significantly stronger than control samples (p < 0.05). Expression of AT2R and MAS receptors were highest with class IIb DN patients. When DN patients were treated with AT1R blocker (ARB), the expression of AT1R was downregulated (p < 0.05), and the MAS receptor was upregulated in tubular interstitial (p < 0.05).Conclusions: Our results directly observed that renal expression levels of AT1R increase during the early stages of DN, ARB reducing AT1R while increasing MAS receptor. Therefore, ARB should be used as soon as possible in patients with DN. [ABSTRACT FROM AUTHOR]

Background: Acute kidney injury in puerperants is generally caused by acute tubular necrosis and occasionally by thrombotic microangiopathy (TMA) following post-partum hemorrhage. However, TMA leads to worse clinical outcomes and is rarely reported in the literature. Therefore, this study aimed to evaluate the pathological mechanism behind the development of TMA in puerperants to improve the diagnosis and treatment of this condition., Methods: Three patients diagnosed with severe postpartum hemorrhage and TMA from 2014 to 2017 at a nephrology center were retrospectively investigated., Results: All patients had severe hemorrhage during delivery with a mean blood loss, 4.0 L (range, 2.7-5.0 L). AKI developed rapidly in these patients and was treated with hemodialysis. Following treatment, the mean volume of packed red blood cells was 2.3 L (range, 1.2-3.6 L), and the mean volume of resuscitation fluid was 3.7 L (range, 3.5-4.0 L). All patients had renal biopsy specimens with typical TMA and ATN changes on light microscopy. Two patients required a hysterectomy while another two patients received respiratory support. Only one patient received plasma exchange. None of the patients had recovered normal kidney function by the final follow-up (26-61 months), with two patients having stage 3 chronic kidney disease, and one patient having an end-stage renal disease requiring maintenance hemodialysis., Conclusion: Severe postpartum hemorrhage could lead to TMA, in addition to the common finding of ATN. Renal histology revealed that poor renal outcomes could be attributed to TMA coexisting with ATN. The potential mechanism was ischemia-reperfusion, which was followed by endothelial cell injury and activation of the alternative complement pathway., Competing Interests: None., (AJTR Copyright © 2021.)

1,25-Dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ) is a secosteroid with antiproliferative property. It also plays a pivotal renoprotective role in diabetic nephropathy. We investigated whether 1,25(OH) 2 D 3 could inhibit the proliferation of rat mesangial cells exposed to high glucose via the DNA-damage-inducible transcript 4/mammalian target of rapamycin(DDIT4/mTOR) pathway. The cell proliferation rate and cell cycle duration were measured using cell counting kit-8 assay and flow cytometry. Protein expression was assayed by Western blot. Glucose acted as a growth factor in rat mesangial cells, promoted cell proliferation. In parallel, the protein expression of DDIT4, TSC1/TSC2, and 4E-BP1 were decreased, and Rheb, mTOR, and p70S6K were increased. Acting via the DDIT4/mTOR signaling, 1,25(OH) 2 D 3 treatment reversed these pathological changes, upregulated DDIT4, TSC1/TSC2, and 4E-BP1, downregulated Rheb, mTOR, and p70S6K. The short-term overexpression of DDIT4 inhibited the proliferation of rat mesangial cells, similar to 1,25(OH) 2 D 3 treatment. siRNA knockdown of DDIT4 suppressed antiproliferative responses to 1,25(OH) 2 D 3 . These results suggest that 1,25(OH) 2 D 3 inhibits the proliferation of rat mesangial cells induced by high glucose via the DDIT4/mTOR signaling pathway., Competing Interests: CONFLICTS OF INTEREST The authors declare that there are no conflicts of interest in this work.

15-year-old boy was admitted with nephritic and nephrotic syndrome, renal dysfunction and decreased serum C3, who suffered from varicella for two months. His renal histopathology revealed endocapillary proliferative glomerulonephritis with podocytes proliferation and severe tubular injury by light microscopy. Direct immunofluorescence showed global granular deposition of IgG, IgA, IgM, C3, C1q and fibrinogen in mesangium and along glomerular capillary wall. Electron microscopic examination showed electron-dense deposits in multiple sites of glomeruli. Furthermore, specific serum IgM antibodies against varicella-zoster virus (VZV) were detected. VZV antigen and mRNA were demonstrated in glomerular and tubular epithelial cells by immunohistochemical staining and in-situ hybridization. Virus particles and virus inclusions were identified by electron microscopy and special staining (Methylene Blue and Eosion staining or Mann staining). The patient also experienced epileptic episodes and his brain MRI and electroencephalogram indicated herpes encephalitis with secondary epilepsy. Therefore, the diagnosis of VZV-associated glomerulonephritis and encephalitis was established. This is the first case of VZV-associated glomerulonephritis with renal histopathological evidence using in situ hybridization technique.

Objective: To analyze clinical and pathologic features of a rare vascular amyloid deposits of amyloid nephropathy (VADAN) in 6 patients, so as to improve its diagnosis and treatment., Methods: All patients received immunopathology, microscopy and electron microscopy examination, and amyloid types were analyzed., Results: There were 3 males and 3 females with ages ranging from 52 to 73 years. Two patients suffered from multiple myeloma. Majority patients had slight albuminuria and hematuria. One patient combined with minimal change glomerular disease presented nephrotic syndrome. One patient combined with IgA nephropathy had albuminuria and hematuria. And one patient had myeloma cast nephropathy with acute renal failure. Kidney biopsy proved amyloid deposits along interlobular arterial wall only in all 6 patients. Two cases secondary from multiple myeloma were κ amyloid, and the rests were λ amyloid., Conclusions: VADAN is a rare type of amyloid nephropathy. Its clinical manifestation is different from common amyloid nephropathy. Kidney biopsy will benefit its differential diagnosis.