Spontaneous renal rupture caused by factor VII deficiency: A case report.

RATIONALE: Spontaneous renal rupture is an uncommon disease, it usually occurs after upper urinary calculi-related operation treatment or renal tumor. This disease caused by factor VII deficiency has rarely reported. PATIENT CONCERNS: A 49-year-old woman came to our hospital with on the left flank pain and gross hematuria that had persisted for 10 days. The patient had no recent history of waist and abdominal trauma or surgical history recently. DIAGNOSES: An outside computed tomography (CT) examination revealed left renal rupture before arriving at our hospital, but she was not treated. Further laboratory examination revealed that the patient condition was turned out to be hemophilia caused by factor VII deficiency. INTERVENTION: We have used both internal and external drainage methods, and supplemented with coagulation factor. OUTCOME: After 9 months of follow-up, it was observed that the left renal hematoma and urinary extravasation was completely absorbed. LESSONS: Spontaneous renal rupture for hemophilia is a clinical emergency. When spontaneous renal rupture is associated with abnormal coagulation function, and the coagulation function cannot be corrected by conventional treatment, the possibility of hemophilia needs to be considered, and the type of hemophilia needs to be further defined. This case indicates a successful resolution of spontaneous renal rupture, it can provide guiding value for our clinical practice.

Exploiting the neonatal crystallizable fragment receptor to treat kidney disease.

The neonatal Fc receptor (FcRn) was initially discovered as the receptor that allowed passive immunity in newborns by transporting maternal IgG through the placenta and enterocytes. Since its initial discovery, FcRn has been found to exist throughout all stages of life and in many different cell types. Beyond passive immunity, FcRn is necessary for intrinsic albumin and IgG recycling and is important for antigen processing and presentation. Given its multiple important roles, FcRn has been utilized in many disease treatments including a new class of agents that were developed to inhibit FcRn for treatment of a variety of autoimmune diseases. Certain cell populations within the kidney also express high levels of this receptor. Specifically, podocytes, proximal tubule epithelial cells, and vascular endothelial cells have been found to utilize FcRn. In this review, we summarize what is known about FcRn and its function within the kidney. We also discuss how FcRn has been used for therapeutic benefit, including how newer FcRn inhibiting agents are being used to treat autoimmune diseases. Lastly, we will discuss what renal diseases may respond to FcRn inhibitors and how further work studying FcRn within the kidney may lead to therapies for kidney diseases.

Association of BKV viremia and nephropathy with adverse alloimmune outcomes in kidney transplant recipients.

BACKGROUND: Immunosuppression reduction for BK polyoma virus (BKV) must be balanced against risk of adverse alloimmune outcomes. We sought to characterize risk of alloimmune events after BKV within context of HLA-DR/DQ molecular mismatch (mMM) risk score. METHODS: This single-center study evaluated 460 kidney transplant patients on tacrolimus-mycophenolate-prednisone from 2010-2021. BKV status was classified at 6-months post-transplant as "BKV" or "no BKV" in landmark analysis. Primary outcome was T-cell mediated rejection (TCMR). Secondary outcomes included all-cause graft failure (ACGF), death-censored graft failure (DCGF), de novo donor specific antibody (dnDSA), and antibody-mediated rejection (ABMR). Predictors of outcomes were assessed in Cox proportional hazards models including BKV status and alloimmune risk defined by recipient age and molecular mismatch (RAMM) groups. RESULTS: At 6-months post-transplant, 72 patients had BKV and 388 had no BKV. TCMR occurred in 86 recipients, including 27.8% with BKV and 17% with no BKV (p = .05). TCMR risk was increased in recipients with BKV (HR 1.90, (95% CI 1.14, 3.17); p = .01) and high vs. low-risk RAMM group risk (HR 2.26 (95% CI 1.02, 4.98); p = .02) in multivariable analyses; but not HLA serological MM in sensitivity analysis. Recipients with BKV experienced increased dnDSA in univariable analysis, and there was no association with ABMR, DCGF, or ACGF. CONCLUSIONS: Recipients with BKV had increased risk of TCMR independent of induction immunosuppression and conventional alloimmune risk measures. Recipients with high-risk RAMM experienced increased TCMR risk. Future studies on optimizing immunosuppression for BKV should explore nuanced risk stratification and may consider novel measures of alloimmune risk.

Comparison of Complications between Total Intravenous Anaesthesia and Combined Intravenous and Inhalation Anaesthesia after Renal Biopsy in Children.

OBJECTIVE: The objective of this study was to examine the influence of total intravenous anaesthesia (TIVA) compared to combined intravenous and inhalation anaesthesia (CIIA) in paediatric patients undergoing renal biopsy. METHODS: A total of 86 children with nephrotic syndrome, acute glomerulonephritis, chronic glomerulonephritis, IgG nephropathy, systemic lupus erythematosus and purpura nephritis were selected from January 2018 to January 2023 in our hospital. All children were divided into the total intravenous anaesthesia group and intravenous inhalational anaesthesia group according to the anaesthesia method. The experimental group comprised 46 children with renal diseases who underwent static aspiration compound anaesthesia during renal biopsy at our hospital from January 2018 to January 2023. Conversely, the control group included 40 children with renal diseases who underwent total intravenous anaesthesia during renal biopsy at the hospital within the same period. Hemodynamic parameters, such as mean arterial pressure (MAP), heart rate (HR), and oxygen saturation (SPO2), were assessed at four different time points: Before anesthesia induction (T0), during anesthesia induction (T1), after anesthesia induction (T2), and at the conclusion of the surgery (T3). Puncture success rate, time to renal puncture, time to get out of bed, postoperative recovery from anaesthesia (including time to postoperative awakening and time to return to spontaneous respiration) and incidence of adverse anaesthetic reactions were also included. RESULTS: We observed notable variations in HR and MAP at T2 and T3, as well as SPO2 levels, duration of awakening from anaesthesia and time taken to resume spontaneous respiration between the two groups at T2 (p < 0.05). No statistically significant variances were detected between the two groups concerning adverse reactions to anaesthesia, puncture success rate, duration to renal puncture and time to mobilisation from bed (p > 0.05). CONCLUSIONS: In conclusion, compared with the total intravenous anaesthesia, the implementation of the sedation-aspiration-combined anaesthesia in renal biopsy in children with renal disease features less haemodynamic fluctuation, better postoperative anaesthesia recovery and does not increase the incidence of adverse reactions.

[Clinical features and death risk factors of pneumocystis jirovecii pneumonia in kidney disease patients with immunosuppressive therapy].

To investigate the clinical features and death risk factors of pneumocystis jirovecii pneumonia (PJP) in kidney disease patients with immunosuppressive patients. A Retrospective case series study was performed in 52 PJP patients with kidney disease who received immunosuppressive therapy in Nephrology or Respiratory department of Peking University First Hospital from January 1, 2006 to August 31, 2021. Patients were divided into survival group (36 cases) and death group (16 cases) according to their clinical outcomes. Univariate analysis was performed to compare the differences of clinical features between the two groups. Multivariate logistic regression model was used to analyze the death risk factors. The results showed that the median serum creatinine was 192.5 (109.8, 293.7) µmol/L, and the incidence of acute kidney injury was 63.5% (33/52). Univariate analysis showed that age (t=1.197,P=0.030), C-reactive protein level (t=2.378,P=0.022), time from onset to diagnosis (χ2=6.62,P=0.010), PJP severity (χ2=5.482,P=0.019), complicated with septic shock (χ2=3.997,P=0.046), mechanical ventilation (χ2=11.755,P=0.001), and blood purification therapy (χ2=4.748,P=0.029) were statistically significant. There were no statistically significant differences between the two groups in gender, duration and dosage of hormone therapy before PJP onset, intravenous methylprednisolone pulse therapy, immunosuppressant use, and serum creatinine level before and after hospitalization for anti-PJP treatment (all P>0.05). Multivariate analysis showed that the time from onset to diagnosis of PJP was >10 days (OR=40.945, 95%CI: 1.738-451.214; P=0.021) and severe PJP (OR=25.502, 95%CI: 1.426-74.806; P=0.028) was an independent death risk factor for kidney disease complicated with PJP of immunosuppressive therapy. In conclusion, the time from onset to diagnosis of PJP and PJP severity are independent death risk factors in patients with kidney disease complicated with PJP of immunosuppressive therapy. Close attention should be paid to oxygenation condition and early diagnosis can prevent the aggravation of PJP and improve the prognosis.

Protective effect of coenzyme Q10 in cyclophosphamide-induced kidney damage in rats.

OBJECTIVE: We aimed to investigate the effect of coenzyme q10 on cyclophosphamide-induced kidney damage in rats. METHODS: A total of 30 female Wistar-Albino rats were utilized to form three groups. In group 1 (control group) (n=10), no drugs were given. In group 2 (cyclophosphamide group) (n=10), 30 mg/kg intraperitoneal cyclophosphamide was administered for 7 days. In group 3 (cyclophosphamide+coenzyme q10 group) (n=10), 30 mg/kg cyclophosphamide and 10 mg/kg coenzyme q10 were given for 7 days via intraperitoneal route. Right kidneys were removed in all groups. Blood malondialdehyde levels and activities of catalase and superoxide dismutase were measured. Histopathological damage was evaluated by examining the slides prepared from kidney tissue using a light microscope. RESULTS: Tissue damage was significantly higher in the cyclophosphamide group than in the cyclophosphamide+coenzyme q10 group (p<0.05). The malondialdehyde levels were significantly higher and the activities of superoxide dismutase and catalase were lower in the cyclophosphamide group than in the cyclophosphamide+coenzyme q10 group (p<0.05). CONCLUSION: Coenzyme q10 may be a good option to prevent cyclophosphamide-induced kidney damage.

Mice with NOP2/sun RNA methyltransferase 5 deficiency die before reaching puberty due to fatal kidney damage.

BACKGROUND: NOP2/Sun RNA methyltransferase 5 (NSUN5) is an RNA methyltransferase that has a broad distribution and plays critical roles in various biological processes. However, our knowledge of the biological functions of NSUN5 in mammals is very limited. Therefore, in this study, we investigate the role of NSUN5 in mice. METHODS: In the present research, we built a mouse model (Nsun5-/-) using the CRISPR/Cas9 system to investigated the specific role of NSUN5. RESULTS: We observed that Nsun5-/- mice had a reduced body weight compared to wild-type mice. Additionally, their survival rate gradually decreased to 20% after postnatal day (PD) 21. Further examination revealed the Nsun5-/- mice had multiple organ damage, with the most severe damage occurring in the kidneys. Moreover, we observed glycogen deposition and fibrosis, along with a notable shorting of the primary foot processes of glomeruli in Nsun5-/- kidneys. Furthermore, we found that the kidneys of Nsun5-/- mice showed increased expression of the apoptotic signal Caspase-3 and accumulated stronger DNA damage at PD 21. CONCLUSIONS: In our study, we found that mice lacking NSUN5 died before puberty due to kidney fatal damage caused by DNA damage and cell apoptosis. These results suggest that NSUN5 plays a vital role in preventing the accumulation of DNA damage and cell apoptosis in the kidney.

Comparison of preventive effects of combined furosemide and mannitol versus single diuretics, furosemide or mannitol, on cisplatin-induced nephrotoxicity.

Cisplatin (CDDP)-induced nephrotoxicity is a common dose-limiting toxicity, and diuretics are often administered to prevent nephrotoxicity. However, the efficacy and optimal administration of diuretics in preventing CDDP-induced nephrotoxicity remain to be established. This study aimed to evaluate the efficacy of combining furosemide and mannitol to prevent CDDP-induced nephrotoxicity. This was a post-hoc analysis of pooled data from a multicenter, retrospective, observational study, including 396 patients who received one or two diuretics for CDDP-based chemotherapy, compared using propensity score matching. Multivariate logistic regression analyses were used to identify risk factors for nephrotoxicity. There was no significant difference in the incidence of nephrotoxicity between the two groups (22.2% vs. 28.3%, P = 0.416). Hypertension, CDDP dose ≥ 75 mg/m2, and no magnesium supplementation were identified as risk factors for nephrotoxicity, whereas the use of diuretics was not found to be a risk factor. The combination of furosemide and mannitol showed no advantage over a single diuretic in preventing CDDP-induced nephrotoxicity. The renal function of patients receiving CDDP-based chemotherapy (≥ 75 mg/m2) and that of those with hypertension should be carefully monitored. Magnesium supplementation is important for these patients.

Midkine promotes renal fibrosis by stabilizing C/EBPß to facilitate endothelial-mesenchymal transition.

Numerous myofibroblasts are arisen from endothelial cells (ECs) through endothelial to mesenchymal transition (EndMT) triggered by TGF-ß. However, the mechanism of ECs transforms to a different subtype, or whether there exists an intermediate state of ECs remains unclear. In present study, we demonstrate Midkine (MDK) mainly expressed by CD31 + ACTA2+ECs going through partial EndMT contribute greatly to myofibroblasts by spatial and single-cell transcriptomics. MDK is induced in TGF-ß treated ECs, which upregulates C/EBPß and increases EndMT genes, and these effects could be reversed by siMDK. Mechanistically, MDK promotes the binding ability of C/EBPß with ACTA2 promoter by stabilizing the C/EBPß protein. In vivo, knockout of Mdk or conditional knockout of Mdk in ECs reduces EndMT markers and significantly reverses fibrogenesis. In conclusion, our study provides a mechanistic link between the induction of EndMT by TGF-ß and MDK, which suggests that blocking MDK provides potential therapeutic strategies for renal fibrosis.

Human Adipose Tissue-Derived Stromal Cells Ameliorate Adriamycin-Induced Nephropathy by Promoting Angiogenesis.

This study is to investigate the therapeutical effect and mechanisms of human-derived adipose mesenchymal stem cells (ADSC) in relieving adriamycin (ADR)-induced nephropathy (AN). SD rats were separated into normal group, ADR group, ADR+Losartan group (20 mg/kg), and ADR + ADSC group. AN rats were induced by intravenous injection with adriamycin (8 mg/kg), and 4 d later, ADSC (2 × 105 cells/mouse) were administrated twice with 2 weeks interval time (i.v.). The rats were euthanized after the 6 weeks' treatment. Biochemical indicators reflecting renal injury, such as blood urea nitrogen (BUN), neutrophil gelatinase alpha (NGAL), serum creatinine (Scr), inflammation, oxidative stress, and pro-fibrosis molecules, were evaluated. Results demonstrated that we obtained high qualified ADSCs for treatment determined by flow cytometry, and ADSCs treatment significantly ameliorated renal injuries in DN rats by decreasing BUN, Scr and NGAL in peripheral blood, as well as renal histopathological injuries, especially protecting the integrity of podocytes by immunofluorescence. Furthermore, ADSCs treatment also remarkably reduced the renal inflammation, oxidative stress, and fibrosis in DN rats. Preliminary mechanism study suggested that the ADSCs treatment significantly increased renal neovascularization via enhancing proangiogenic VEGF production. Pharmacodynamics study using in vivo imaging confirmed that ADSCs via intravenous injection could accumulate into the kidneys and be alive at least 2 weeks. In a conclusion, ADSC can significantly alleviate ADR-induced nephropathy, and mainly through reducing oxidative stress, inflammation and fibrosis, as well as enhancing VEGF production.

UNC93B1 Mediates the Effects of cGAS-STING on ER Stress and Iron Death, and Reduces Renal Toxicity in Cadmium-Exposed Rats.

BACKGROUND: Long-term exposure to cadmium can induce renal toxicity in rats, leading to endoplasmic reticulum (ER) stress and iron death. Notably, in cadmium-exposed rats, there is an increased expression of UNC93B1 (unc-93 homolog B1). Consequently, our investigation aims to determine the impact of UNC93B1 on ER stress and iron death in cadmium-exposed rats by modulating the cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon genes) pathway. METHODS: A cadmium-exposed rat model was established by intrabacally injecting chromium chloride (5 mg/kg, once a day for 4 weeks), and the levels of UCd (urine cadmium), UNAG (urine N-acetyl-ß-D-glucosaminidase), and UCr (urine creatinine) in urine were assessed. A silent UNC93B1 lentivirus was constructed, and STING agonists were procured and administered to the rats. Subsequently, kidney tissues were extracted post-mortem, and pathological changes in renal tissue were observed through hematoxylin and eosin (HE) staining. The expression and mRNA levels of UNC93B1, cGAS, and STING were examined using western blot (WB) and polymerase chain reaction (PCR). Autophagy proteins (light chain 3 (LC3), Beclin-1, p62) were also assessed by WB. Additionally, iron concentration was determined using a kit, while oxidative stress markers (cytochrome oxidase subunit 2 (COX2), glutathione peroxidase 4 (GPX4), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH)) were measured through enzyme-linked immunosorbent assay (ELISA). Furthermore, endoplasmic reticulum stress proteins (protein kinase RNA-like ER kinase (PERK), CCAAT enhance-binding protein homologous protein (CHOP), activating transcription factor-4 (ATF4)) were analyzed by WB. RESULTS: Wstaining, WB, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), ELISA, and HE staining collectively revealed a heightened expression of UNC93B1, cGAS, and STING, accompanied by increased levels of autophagy, oxidative stress, and ER stress in cadmium-exposed rats (p < 0.05). Nephrotoxicity exhibited a reduction following the inhibition of UNC93B1, leading to decreased levels of oxidative stress, autophagy, and ER stress (p < 0.05). Notably, this observed phenomenon was reversed upon the addition of STING agonists, suggesting that UNC93B1 might exert a nephroprotective effect in cadmium-exposed rats through modulation of the cGAS-STING pathway. CONCLUSIONS: The inhibition of UNC93B1 mitigates nephrotoxicity in cadmium-exposed rats, and this protective effect is mechanistically linked to the cGAS-STING pathway.

Identification and analysis of differently expressed transcription factors in aristolochic acid nephropathy.

BACKGROUND: Aristolochic acid nephropathy (AAN) is a rapidly progressive interstitial nephropathy caused by Aristolochic acid (AA). AAN is associated with the development of nephropathy and urothelial carcinoma. It is estimated that more than 100 million people worldwide are at risk of developing AAN. However, the underlying mechanisms driving renal deterioration in AAN remain poorly understood, and the treatment options are limited. METHODS: We obtained GSE27168 and GSE136276 series matrix data from the Gene Expression Omnibus (GEO) related to AAN. Using the R Studio environment, we applied the limma package and WGCNA package to identify co-differently expressed genes (co-DEGs). By GO/KEGG/GSVA analysis, we revealed common biological pathways. Subsequently, co-DEGs were subjected to the String database to construct a protein-protein interaction (PPI) network. The MCC algorithms implemented in the Cytohubba plugin were employed to identify hub genes. The hub genes were cross-referenced with the transcription factor (TF) database to identify hub TFs. Immune infiltration analysis was performed to identify key immune cell groups by utilizing CIBERSORT. The expressions of AAN-associated hub TFs were verified in vivo and in vitro. Finally, siRNA intervention was performed on the two TFs to verify their regulatory effect in AAN. RESULTS: Our analysis identified 88 co-DEGs through the "limma" and "WGCNA" R packages. A PPI network comprising 53 nodes and 34 edges was constructed with a confidence level >0.4. ATF3 and c-JUN were identified as hub TFs potentially linked to AAN. Additionally, expressions of ATF3 and c-JUN positively correlated with monocytes, basophils, and vessels, and negatively correlated with eosinophils and endothelial cells. We observed a significant increase in protein and mRNA levels of these two hub TFs. Furthermore, it was found that siRNA intervention targeting ATF3, but not c-JUN, alleviated cell damage induced by AA. The knockdown of ATF3 protects against oxidative stress and inflammation in the AAN cell model. CONCLUSION: This study provides novel insights into the role of ATF3 in AAN. The comprehensive analysis sheds light on the molecular mechanisms and identifies potential biomarkers and drug targets for AAN treatment.

OHVIRA syndrome: clinical implications of a delayed diagnosis.

Obstructed Hemi Vagina with Ipsilateral Renal Agenesis (OHVIRA) syndrome is a rarely encountered müllerian duct anomaly. Delayed diagnosis is common due to normal onset of puberty and menstruation. We report a case of a woman in her early 20s with a background history of multiple emergency department visits, ward admissions and surgeries for chronic abdominal pain. She was reviewed at 1 month postlaparotomy for recurrent pelvic abscess and was finally diagnosed to have an OHVIRA syndrome, 11 years after her first clinical presentation. Excision of the vaginal septum completely resolved her symptoms. We are reporting this case to highlight the clinical implications resulting from the delayed diagnosis, to look into factors contributing to the delay and to highlight the importance of having a high index of suspicion to diagnose this unique condition.

Renal candidiasis associated with papillary necrosis in a captive tiger (Panthera tigris).

A 14-year-old male tiger developed anorexia with elevated blood urea nitrogen and creatinine levels. The patient had a palpable abdominal mass and demonstrated neutrophilic leukocytosis and anaemia. Leukocytes, yeast and bacteria were present in the urine. The animal was non-responsive to therapy and was subsequently euthanised. Extensive acute renal papillary necrosis (RPN) with pyelonephritis, chronic nephritis and polycystic renal disease were evident during gross and microscopic pathology examinations. The histologic occurrence of fungal spores and pseudohyphae morphologically consistent with Candida species were observed within the necrotic papillary regions of the kidney and within multiple foci of mild parakeratotic hyperkeratosis present in the gingiva and tongue. Candida albicans along with a slight growth of Escherichia coli were recovered from kidney cultures. Possible contributory factors for the renal candidiasis and associated RPN include predisposing oral candidiasis, polycystic renal disease, ischaemic nephrosclerosis, age-associated or other forms of immunodeficiency and therapy with meloxicam, a non-steroidal anti-inflammatory drug. The absence of apparent lower urinary tract involvement coupled with the presence of intravascular renal 'Candida emboli' suggest that chronic oral candidiasis was the probable source of the kidney infection.

Amino Acids during Pregnancy and Offspring Cardiovascular-Kidney-Metabolic Health.

Amino acids are essential for normal pregnancy and fetal development. Disruptions in maternal amino acid metabolism have been associated with various adult diseases later in life, a phenomenon referred to as the developmental origins of health and disease (DOHaD). In this review, we examine the recent evidence highlighting the significant impact of amino acids on fetal programming, their influence on the modulation of gut microbiota, and their repercussions on offspring outcomes, particularly in the context of cardiovascular-kidney-metabolic (CKM) syndrome. Furthermore, we delve into experimental studies that have unveiled the protective effects of therapies targeting amino acids. These interventions have demonstrated the potential to reprogram traits associated with CKM in offspring. The discussion encompasses the challenges of translating the findings from animal studies to clinical applications, emphasizing the complexity of this process. Additionally, we propose potential solutions to overcome these challenges. Ultimately, as we move forward, future research endeavors should aim to pinpoint the most effective amino-acid-targeted therapies, determining the optimal dosage and mode of administration. This exploration is essential for maximizing the reprogramming effects, ultimately contributing to the enhancement of cardiovascular-kidney-metabolic health in offspring.

Bilateral renal lymphangiectasia: Literature review of a rare entity.

Renal lymphangiectasia (RL) is a rare condition in which lymphatic vessels are dilated giving rise to cyst formation in peripelvic, perirenal and intrarenal locations. Knowledge about RL is limited and based upon individual case reports. This can be genetic or acquired. There is no significant association with any gender or age. It can be manifested as focal or diffuse forms and can be unilateral or bilateral. Most of the cases present with abdominal or flank pain. The diagnosis is based on radiological imaging. Due to rarity of diseases, it has potential to be misdiagnosed as other cystic disease of kidneys. The treatment is mainly conservative but prolonged follow up for associated complications like hypertension and renal vein thrombosis is required. We have presented a case of bilateral renal lymphangiectasia with the review of available literature.

Impact of kidney disease on perioperative outcomes of endoscopic BPH surgery: a propensity score matched analysis from the NSQIP database.

INTRODUCTION: To assess the impact of kidney function in patients with BPH undergoing surgery prior to Transurethral resection of prostate (TURP), Laser enucleation of the prostate (LEP), and Laser Vaporization of the prostate (LVP) on operative and post-operative outcomes using the ACS-NSQIP database. METHODS: The ACS-NSQIP database was reviewed for patients that underwent TURP, LEP and LVP for treatment of patients with BPH between the years of 2008 and 2021. Demographics, comorbidities, bleeding disorders, operative time, and surgical procedure performed were collected for comparison between Kidney function groups: G1, normal/high function; G2-G3, mild/moderate kidney disease; and G4-G5, severe kidney disease. The 30-day peri-operative complications were measured and a multivariate logistic regression analysis was performed while adjusting for all confounding variables. Propensity score matching was performed between the G1 and G4-G5 cohorts. RESULTS: A total of 83,020 patients were included. On multivariable regression, in the G2-G3 cohort, patients were at significantly increased risk for renal complications with OR = 2.43[1.56-3.79]. After propensity score matching, the G4-G5 cohort showed increased odds of pneumonia OR = 4.02[1.343-12.056], renal complications with OR = 7.62[2.283-25.411], cardiac complications OR = 4.53[1.531-13.411], and sepsis/septic shock OR = 1.76[1.091-2.834]. They also had a higher need for blood transfusion OR = 3.58[2.242-5.714], and prolonged hospital stay with OR = 1.49[1.296-1.723]. CONCLUSION: Pre-operative kidney disease may pose an increased risk of complications for patients undergoing endoscopic BPH surgery. The literature lacks information on the effect of pre-operative kidney disease on endoscopic BPH surgeries. Further studies are required to compare post-operative outcomes of LEP and LVP as compared to TURP across kidney function status.

Kefir mitigates renal damage caused by zearalenone in female wistar rats by reducing oxidative stress.

The estrogen-like mycotoxin zearalenone (ZEA) was popularly occurred in several food and feeds, posing threats to human and animal health. ZEA induced renal toxicity and caused oxidative stress. In the current study, the protecting effect of kefir administration against ZEA-induced renal damage in rats was explored. Rats were divided into 4 groups, each consisting of 5 animals. For the initial 7 days, they were orally administered sterile milk (200 µL/day). Subsequently, during the second week, the groups were exposed to kefir (200 µL/day), ZEA (40 mg/kg b.w./day) and a combination of kefir and ZEA. The biochemical parameters, kidney histological changes and ZEA residue were assessed. Kefir supplementation enhanced the antioxidant enzymes in the kidney, such as superoxide dismutase, catalase and glutathione peroxidase activities, which increased by 1.2, 4 and 20 folds, respectively, relative to the ZEA group. Remarkably, the concomitant administration kefir + ZEA suppressed ZEA residues in both serum and kidney. Additionally, serum levels of blood urea nitrogen, uric acid and renal malondialdehyde decreased by 22, 65 and 54%, respectively, in the kefir + ZEA group; while, the creatinine content increased by around 60%. Rats co-treated with kefir showed a normal kidney histological architecture contrary to tissues alterations mediated in the ZEA group. These results suggest that kefir may showed a protective effect on the kidneys, mitigating ZEA-induced acute toxicity in rats.