Renal Histopathological Findings Research Articles

Relationship between MRI findings and renal histopathology in IgG4-related tubulointerstitial nephritis.

MRI is expected to be a valuable tool for evaluating disease activity in immunoglobulin G4 (IgG4)-related tubulointerstitial nephritis (IgG4-TIN). However, the correlation between MRI findings and renal histopathological findings remains to be elucidated. This study aimed to clarify the correlation between MRI findings and renal histopathological findings in IgG4-TIN. This retrospective cross-sectional study investigated 26 patients with biopsy-proven IgG4-TIN who underwent simultaneous percutaneous kidney biopsies and abdominal MRI examinations at Toranomon Hospital or Toranomon Hospital Kajigaya between December 2007 and November 2022. We reviewed kidney biopsy specimens and scored the degree of inflammatory cell infiltration and interstitial fibrosis. We assessed abdominal MRI, specifically examining T1WI, T2WI, and DWI, for the presence of abnormal signals in the inferior pole of the kidney on the side where the kidney biopsy was performed. Spearman's correlation coefficient test was conducted to examine the relationship between the images and histological findings. For T1WI, eight cases showed a positive low-intensity signal, and 18 cases were negative. For T2WI, 19 cases were positive for a low-intensity signal, and seven cases were negative. In DWI, 23 cases were positive for a high-intensity signal, and one was negative. T1WI low-intensity signal and T2WI low-intensity signal were significantly correlated with interstitial fibrosis score (correlation coefficient 0.52 and 0.64). DWI revealed IgG4-TIN detected IgG4-TIN lesions with the highest sensitivity; however, the correlation with inflammatory cell infiltration score was not significant. Low-intensity signal on T2WI is useful for predicting the degree of fibrosis in IgG4-TIN.

Alirocumab boosts antioxidant status and halts inflammation in rat model of sepsis-induced nephrotoxicity via modulation of Nrf2/HO-1, PCSK9/HMGB1/NF-ᴋB/NLRP3 and Fractalkine/CX3CR1 hubs

Acute kidney injury (AKI) is a devastating consequence of sepsis, accompanied by high mortality rates. It was suggested that inflammatory pathways are closely linked to the pathogenesis of lipopolysaccharide (LPS)-induced AKI. Inflammatory signaling, including PCSK9, HMGB1/RAGE/TLR4/MYD88/NF-κB, NLRP3/caspase-1 and Fractalkine/CX3CR1 are considered major forerunners in this link. Alirocumab, PCSK9 inhibitor, with remarkable anti-inflammatory features. Accordingly, this study aimed to elucidate the antibacterial effect of alirocumab against E. coli in vitro. Additionally, evaluation of the potential nephroprotective effects of alirocumab against LPS-induced AKI in rats, highlighting the potential underlying mechanisms involved in these beneficial actions. Thirty-six adult male Wistar rats were assorted into three groups (n=12). Group I; was a normal control group, whereas sepsis-mediated AKI was induced in groups II and III through single-dose intraperitoneal injection of LPS on day 16. In group III, animals were given alirocumab. The results revealed that LPS-induced AKI was mitigated by alirocumab, evidenced by amelioration in renal function tests (creatinine, cystatin C, KIM-1, and NGAL); oxidative stress biomarkers (Nrf2, HO-1, TAC, and MDA); apoptotic markers and renal histopathological findings. Besides, alirocumab pronouncedly hindered LPS-mediated inflammatory response, confirmed by diminishing HMGB1, TNF-α, IL-1β, and caspase-1 contents; the gene expression of PCSK9, RAGE, NF-ᴋB and Fractalkine/CX3CR1, along with mRNA expression of TLR4, MYD88, and NLRP3. Regarding the antibacterial actions, results showed that alirocumab displayed potential anti-bacterial activity against pathogenic gram-negative E. coli. In conclusion, alirocumab elicited nephroprotective activities against LPS-induced AKI via modulation of Nrf2/HO-1, PCSK9, HMGB1/RAGE/TLR4/MYD88/NF-ᴋB/NLRP3/Caspase-1, Fractalkine/CX3R1 and apoptotic axes.

Outcomes Associated with Clone-Directed Therapies for Monoclonal Gammopathy of Renal Significance

Background: Monoclonal Gammopathy of Renal Significance (MGRS) is a category of diseases not meeting criteria for cancer, in which a clonal population of B-lymphoid or plasma cells produces a nephrotoxic protein leading to kidney injury. Informal consensus has arisen that therapy targeting the causal clone is most likely to be efficacious, and the primary goal of therapy is to prolong renal survival. Light chain (AL) amyloidosis has been extensively studied, yet there is a paucity of data describing outcomes associated with clone-directed therapy for the various subtypes of non-AL MGRS. Methods: This was a retrospective analysis of patients treated at two National Cancer Institute (NCI)-designated cancer centers in the United States. Medical records of adult patients seen between January 2010 and March 2023 were screened for MGRS. Patients were eligible if they had renal biopsy-confirmed histopathologic findings compatible with MGRS. AL amyloidosis was excluded. The primary outcome was renal survival, defined as time from diagnosis of MGRS to requiring renal replacement therapy (RRT) or renal transplant, with patients censored at last follow up or death. Baseline characteristics were described, including 24-hour proteinuria, estimated glomerular filtration rate (eGFR), whether a clonal population of B cells or plasma cells could be identified on histopathologic examination of marrow or lymph node biopsy, concentration of monoclonal protein, and involved serum free light chain concentration. Initial therapy was reported, although differences in outcomes across therapeutic strategies were not compared. Baseline clinical characteristics between patients who required RRT and those who did not were compared. Baseline clinical variables and time to RRT were compared across the two most common MGRS subtypes in the cohort: proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) and light chain deposition disease (LCDD). Continuous variables were compared across subgroups using Wilcoxon rank-sum test. Time-to-event outcomes were analyzed according to the Kaplan-Meier method. All analyses were conducted using R version 3.6.1. Results: In total, 65 patients were included, 23 (35%) of whom ultimately required RRT or transplant. Four patients died, all after RRT. Median baseline proteinuria was 2802 mg/24h (IQR 972.5 - 4492.0) and median eGFR was 33.0 mL/min (IQR 23 - 53) for the entire cohort. In all cases proteinuria was mostly albumin. Median baseline involved light chain concentration was 8.3 mg/dL (IQR 3.1 - 26.4). A majority of patients (n=33, 51%) had no identifiable serum monoclonal protein. The two most common MGRS subtypes were PGNMID (n = 26) followed by LCDD (n = 21). Clonal populations thought to be causing MGRS were identified in 41/64 patients (64%), including 37 (58%) with plasma cell clones, 1 (2%) with a lymphoplasmacytic lymphoma clone, and 3 (4.7%) with other B-cell clones. Clones were not identified in 23 (36%). The most common chemotherapy agents included bortezomib (n=42, 64%) and rituximab (n=14, 22%). Compared to patients not requiring RRT, patients requiring RRT had higher baseline proteinuria (median 3531 vs. 1980 mg/24h, p<0.001) and lower eGFR (median 16 v. 44 mL/min, p<0.001); differences in serum free light chain concentrations were not significant ( Figure 1). A clonal population thought to be causing MGRS was identified on bone marrow biopsy in a majority of LCDD patients (n = 20, 95%), while clones were infrequently found in PGNMID (n = 6, 23%). The vast majority (n=20, 95%) of patients with LCDD received bortezomib-based therapy. Initial therapy in patients with PGNMID was more evenly divided: 9 (35%) received bortezomib-based therapy, 10 (38%) received rituximab-based therapy, and 6 (23%) received other regimens. Despite differences in therapeutic approach, patients with LCDD and in patients with PGNMID had similar risk of RRT (cumulative risk 35% v. 43%, p=0.54; HR 0.83 (95% CI 0.52-1.33); p =0.44) ( Figure 2). Conclusion: Patients with MGRS remain at high risk of requiring RRT even with clone-directed therapy. Despite differences in pathogenic clones and therapeutic strategies, outcomes of patients with PGNMID and LCDD are similar. Because the severity of baseline renal function across MGRS histologies predicts renal survival, early diagnosis and treatment is likely critical to improving renal outcomes.

Kidney histopathology in predicting flares following drug withdrawal in proliferative lupus nephritis in clinical remission.

Residual renal histopathological activity at clinical remission in Proliferative Lupus Nephritis (PLN) can predict renal flare upon immunosuppression withdrawal. Data on the role of histological renal remission in predicting extra-renal flares is lacking. We assessed renal histopathology prior to drug withdrawal and the occurrence of renal and extra-renal flares over 52weeks after drug withdrawal in PLN patients in long-term clinical remission. This is a subgroup analysis of a non-inferiority, open-label randomized (1:1) controlled trial. Patients with biopsy-proven Class III/IV LN in the past (biopsy 1), on immunosuppressants (IS) ≥ 3years, in clinical remission for ≥ 1year, on stable prednisolone dose (≤ 7.5mg/day) plus a maintenance IS and hydroxychloroquine (HCQ) were subjected to a repeat renal biopsy (biopsy 2). Individuals with biopsy 2 having activity index (AI) < 4/24 were randomised to either prednisolone or IS withdrawal. Primary end-point was the proportion experiencing a flare [SELENA-SLEDAI flare index (SFI)] at week 52. Twenty-eight eligible patients underwent biopsy 2 and randomized to prednisolone (n = 15) and IS (n = 13) withdrawal. At biopsy 1, 12 (43%) had class III, 15 (53.5%) had class IV, and 1 (3.5%) had class III + V. At biopsy 2, PLN persisted in 4 (14.2%) while 18 (64.2%) were in histological remission (AI = 0) with 6(21.4%) in class II. Following drug withdrawal, 9/28 (32%) had flares especially musculoskeletal (55.5%), mucocutaneous (44.4%), and renal (33.3%). Among the four persistent PLN patients, one of the two (50%) with AI = 1 had extra-renal flare while both the two with AI = 2 (100%) had renal and extra-renal flares. In those with histological remission (biopsy 2), 6/18 (66.6%) experienced extra-renal flare of whom one also had renal flare. Upon drug withdrawal, renal histopathology findings with any activity index can predict renal flare while histological remission is not enough to predict extra-renal flare, thus making it an unsuitable marker for deep SLE remission.

Coenzyme Q10-Loaded Albumin Nanoparticles Protect against Redox Imbalance and Inflammatory, Apoptotic, and Histopathological Alterations in Mercuric Chloride-Induced Hepatorenal Toxicity in Rats.

Exposure to mercuric chloride (HgCl2), either accidental or occupational, induces substantial liver and kidney damage. Coenzyme Q10 (CoQ10) is a natural antioxidant that also has anti-inflammatory and anti-apoptotic activities. Herein, our study aimed to investigate the possible protective effects of CoQ10 alone or loaded with albumin nanoparticles (CoQ10NPs) against HgCl2-induced hepatorenal toxicity in rats. Experimental animals received CoQ10 (10 mg/kg/oral) or CoQ10NPs (10 mg/kg/oral) and were injected intraperitoneally with HgCl2 (5 mg/kg; three times/week) for two weeks. The results indicated that CoQ10NP pretreatment caused a significant decrease in serum liver and kidney function markers. Moreover, lowered MDA and NO levels were associated with an increase in antioxidant enzyme activities (SOD, GPx, GR, and CAT), along with higher GSH contents, in both the liver and kidneys of intoxicated rats treated with CoQ10NPs. Moreover, HgCl2-intoxicated rats that received CoQ10NPs revealed a significant reduction in the hepatorenal levels of TNF-α, IL-1β, NF-κB, and TGF-β, as well as an increase in the hepatic level of the fibrotic marker (α-SMA). Notably, CoQ10NPs counteracted hepatorenal apoptosis by diminishing the levels of Bax and caspase-3 and boosting the level of Bcl-2. The hepatic and renal histopathological findings supported the abovementioned changes. In conclusion, these data suggest that CoQ10, alone or loaded with albumin nanoparticles, has great power in reversing the hepatic and renal tissue impairment induced by HgCl2 via the modulation of hepatorenal oxidative damage, inflammation, and apoptosis. Therefore, this study provides a valuable therapeutic agent (CoQ10NPs) for preventing and treating several HgCl2-induced hepatorenal disorders.

Significance of co-positivity for anti-dsDNA, -nucleosome, and -histone antibodies in patients with lupus nephritis

Objective The aim of this study was to define the clinical, histopathologic, and prognostic features associated with simultaneous positivity for anti-dsDNA, -nucleosome, and -histone antibodies (3-pos) in Korean patients with biopsy-proven lupus nephritis (LN). Methods The 102 patients included in the study had undergone kidney biopsy prior to the start of induction treatment, were treated with immunosuppressives, and followed-up for >12 months. Results In total, 44 (43.1%) of the 102 LN patients were 3-pos. Patients with 3-pos had a higher SLEDAI-2K score (p = .002), lower lymphocyte count (p = .004), and higher rates of proteinuria > 3.5 g/24 h (p = .039) and positivity for urinary sediments (p = .005) at the time of renal biopsy than non-3-pos patients. 3-pos patients had a more proliferative form of LN (p = .045) in the renal histopathologic findings, and as co-positivity gradually increased from 0 to 3, the total activity score in the renal biopsy findings increased significantly (p = .033). In addition, 3-pos patients had a more rapid eGFR decline than non-3-pos patients after a follow-up of 83.2 months (p = .016). Conclusions Our findings suggest that 3-pos is related to severe LN and that 3-pos patients are more likely to experience a rapid decline of renal function than non-3-pos patients. KEY MESSAGE Patients with co-positivity for anti-dsDNA, -nucleosome, and -histone antibodies (3-pos) had higher disease activity and a worse renal histopathology than those without co-positivity. 3-pos patients had a more rapid decline of renal function than non-3-pos patients.

Bone marrow mesenchymal stem cells inhibit ferroptosis via regulating the Nrf2-keap1/p53 pathway to ameliorate chronic kidney disease injury in the rats

Purpose Although bone marrow mesenchymal stem cells (BMMSCs) have been reported to exhibit a protective effect on animal models of chronic kidney disease (CKD), the exact mechanisms involved require further investigation. This study aims to investigate the underlying molecular mechanisms of BMMSCs in inhibiting ferroptosis and preventing an Adriamycin (ADR)-induced CKD injury. Methods A rat model of long-term CKD induced through the injection of ADR administered twice weekly via the tail vein was used in this study. After BMMSCs were systemically administered through the renal artery, pathological staining, western blotting, ELISA, and transmission electron microscopy were used to analyze ferroptosis. Results Analyses of renal function and histopathological findings indicated that ADR-mediated renal dysfunction improved in response to the BMMSC treatment, which was also sufficient to mediate the partial reversal of renal injury and mitochondrial pathological changes. BMMSCs decreased the ferrous iron (Fe2+) and reactive oxygen species and elevated glutathione (GSH) and GSH peroxidase 4. Moreover, the BMMSC treatment activated the expression of ferroptosis-related regulator NF-E2-related factor 2 (Nrf2) and inhibited Keap1 and p53 in CKD rat kidney tissues. Conclusions BMMSCs alleviate CKD, possibly resulting from the inhibition of kidney ferroptosis by regulating the Nrf2–Keap1/p53 pathway.

U-KIM-1 as a predictor of treatment response in lupus nephritis.

Biomarkers of disease activity in lupus nephritis (LN) are in demand. This is because they may be useful in patients who are unable to undergo invasive kidney biopsy, as predictors of renal function, and for early detection of LN recurrence. The focus is on the measurement of urinary chemokines and cytokines, especially in urinary biomarkers, which are non-invasive and simple. In our previous report, we reported that kidney injury molecule-1 (KIM-1) is expressed in injured tubules and that the number of tubular-KIM-expressing positive cells correlates with renal pathology findings and also with urinary (u)-KIM-1 levels. However, there have been no reports examining the effect of u-KIM-1 levels on response to therapy, correlation with renal pathology, and usefulness as a predictor of renal function. U-KIM-1 levels were measured by ELISA in 61 SLE patients. In 38 active LN who underwent renal biopsy, we also examined whether u-KIM-1 levels affected LN disease activity, renal histological findings, and predictors of renal function. In SLE patients, proteinuria and u-KIM-1 levels were elevated in active LN compared to inactive LN. U-KIM-1 and proteinuria decreased with intensified treatment. U-KIM-1 levels also correlated with the percentage of glomerular crescent formation in renal pathology. In addition, patients with higher baseline u-KIM-1 levels had significantly higher eGFR and lower LN disease activity at 12months after treatment intensification. These data suggest that u-KIM-1 levels correlate with LN disease activity and renal histopathology findings and may be used as a predictor of treatment response.

POS-125 Revisiting kidney injury in scrub typhus infection: A novel cause of infection-related glomerulonephritis

Kidney injury related to infections is one of the important preventable causes of morbidity and mortality, especially in tropical regions. Kidney involvement in scrub typhus infection ranges from bland urinary sediments to the requirement of renal replacement therapy (RRT). Earlier studies have shown renal histopathological findings consistent with acute tubular necrosis, interstitial nephritis, and mild mesangial glomerulonephritis in patients with scrub typhus and renal injury. We investigated patients with complicated scrub typhus for the pattern of renal involvement.

Endocapillary hypercellularity levels are associated with early complete remission in children with class IV lupus nephritis as the initial presentation of SLE

BackgroundEndocapillary hypercellularity (ECHC) is commonly seen in class IV lupus nephritis (LN), the most common and severe LN in children. Factors influencing early complete remission (CR) in pediatric class IV LN have been poorly described. We investigated the relationship between ECHC levels and early CR in pediatric class IV LN.MethodsPatients with newly, simultaneously diagnosed systemic lupus erythematosus (SLE) and class IV LN by renal biopsy from 2012 to 2021 were studied. In this retrospective study, two pathologists who were blind to clinical information reviewed all pathological data retrospectively and classified glomerular lesions according to the revised criteria of the International Society of Nephrology and the Renal Pathology Society (ISN/RPS). The demographics, baseline clinical characteristics, laboratory parameters, renal histopathological findings, treatment regimen and CR at 6 months after immunosuppressive therapy were analyzed. ECHC was categorized as: > 50% (group A), 25–50% (group B) and < 25% (group C). CR was defined as absence of clinical symptoms, 24-hour urinary protein < 0.15 g, and normal levels of serum creatinine and albumin.ResultsSixty-four patients were identified: 23, 15 and 26 in groups A, B and C, respectively. Group A had significantly higher levels of D-dimer, urine protein, and SLE disease activity index (SLEDAI) than groups B and C. Group C had a markedly higher estimated glomerular filtration rate (eGFR) than groups A and B. A substantially greater proportion of patients in group A had glomerular microthrombi and basement membrane thickening than in groups B and C. At 6 months post treatment, CR was achieved in 19 (82.6%), 5 (33.3%) and 11 (42.3%) in groups A, B and C, respectively (p < 0.05, group A vs groups B and C). Multiple logistic regression analysis revealed that ECHC and urine protein levels were significantly associated with CR.ConclusionECHC and urine protein levels may be valuable biomarkers for predicting early CR in pediatric class IV LN.

Identification of histopathological and clinical spectrum of diabetic kidney disease based on an unsupervised hierarchical clustering analysis of elderly autopsy specimens.

Diabetic kidney disease (DKD), a chronic kidney disease caused by diabetes and other comorbidities, is the leading cause of end-stage renal disease. The pathogenesis of DKD is diverse and influenced by various causes, some but not all of which cause proteinuria. Some factors such as hypertension can modify DKD. Therefore, the spectrum of DKD is difficult to elucidate and remains unsolved. This study aims to classify and characterize DKD. We examined autopsy specimens from type 2 diabetes mellitus (DM) (n=44) and non-DM (n=21) groups. The frequency of interstitial fibrosis and tubular atrophy was higher in patients with proteinuric DKD than in those with non-proteinuric DKD. The presence of polar vasculosis was associated with hypertension in DKD. In addition, an unsupervised hierarchical clustering analysis revealed the spectrum of renal histopathology findings for more-proteinuric and less-proteinuric DKD. With changes in the diagnostic criteria for hypertension and advances in antihypertensive drugs, the pathogenesis of DKD may be changing. Furthermore, a decision tree model suggested how diabetes, hypertension, and dyslipidemia interacted in predicting the characteristics of DKD. Polar vasculosis is a good indicator of the presence of DM and hypertension. Furthermore, the histopathological and clinical spectrum of DKD were related to the interaction of diabetes, hypertension, and dyslipidemia. These histopathological and clinical results may help to show the range of patient characteristics when conducting clinical trials and could help to determine whether chronic kidney disease is caused by DM or some other cause.

Histopathological features of kidney and renal prognosis in patients with preeclampsia

Understanding the long-term prognosis of preeclampsia (PE) is important. Proteinuria and poor renal function persist in some PE patients, but the relationship between their histopathological findings of kidney and renal prognosis is unknown. Our objective was to clarify the relationship between clinicopathological features and renal prognosis in PE patients. Retrospective observational study. Seventy patients who had been referred to the Niigata University Hospital between 1977 and 2014 and were diagnosed with PE were classified into unimproved and improved groups. The unimproved group included patients whose serum creatinine level had doubled and/or whose proteinuria had persisted until the end of observation, which included three patients with end-stage kidney disease (ESKD). The improved group included patients whose serum creatinine level did not double and whose proteinuria had disappeared until the last observation. We examined and compared these patients' characteristics, clinical and laboratory findings, and renal histopathological findings from percutaneous kidney biopsies. There were no significant differences in the clinical backgrounds and clinical findings between the two groups during pregnancy. However, light microscopy findings of their kidney biopsies were able to identify significantly more severe duplications of the capillary loop, interstitial cell infiltration, and interstitial fibrosis in the unimproved group. Histopathological examination of the kidney may be a valid method for predicting the long-term prognosis of renal function and for histological a risk assessment of poor renal recovery in PE patients.

Clinical Presentation, Renal Histopathological Findings, and Outcome in Patients with Monoclonal Gammopathy and Kidney Disease.

Monoclonal gammopathies are associated with acute and chronic kidney injury. Nephrotoxicity of the secreted monoclonal (M)-protein is related to its biological properties and blood concentration. Little is known about epidemiology, clinical manifestations, and outcome of monoclonal gammopathies in patients with kidney disease. We retrospectively collected data about demographics, clinical manifestations, and renal histological lesions of all patients (n = 1334) who underwent kidney biopsy between January 2000 and March 2017. Monoclonal gammopathy was detected in 174 (13%) patients with a mean age of 66.4 ± 13.1 years. The spectrum of monoclonal gammopathies comprised monoclonal gammopathy of undetermined significate (MGUS) (52.8%), multiple myeloma (MM) (25.2%), primary amyloidosis (AL) (9.1%), smoldering MM (SMM) (4%), non-Hodgkin lymphoma (NHL) (6.8%), and Hodgkin lymphoma (HL) (1.7%). Monoclonal gammopathy of renal significance (MGRS) accounted for 6.5% in patients with MGUS and 14.2% in patients with SMM. Evaluation of kidney biopsy revealed that M-protein was directly involved in causing kidney injury in MM (93.1%). MM was the only gammopathy significantly associated with an increased risk of kidney injury (odds ratio [OR] = 47.5, CI 95%, 13.7–164.9; P ≤ 0.001). While there were no significant differences in the progression toward end-stage renal disease or dialysis (P = 0.776), monoclonal gammopathies were associated with a different risk of death (P = 0.047) at the end of the follow-up. In conclusion, monoclonal gammopathy was a frequent finding (13%) in patients who underwent kidney biopsy. M-protein was secreted by both premalignant (56.8%) and malignant (43.2%) lymphoproliferative clones. Kidney biopsy had a key role in identifying MGRS in patients with MGUS (6.5%) and SMM (14.2%). Among monoclonal gammopathies, only MM was significantly associated with biopsy-proven kidney injury. The rate of end-stage renal disease or dialysis was similar among monoclonal gammopathies, whereas NHL, MM, and SMM showed a higher rate of deaths.

Multidisciplinary approach in the diagnosis of acute leptospirosis in dogs naturally infected by Leptospira interrogans serogroup Icterohaemorrhagiae: A prospective study

Leptospirosis, a zoonotic disease with worldwide distribution, is caused by spirochetes of the genus Leptospira. In dogs, this disease is frequently misdiagnosed. Few studies have attempted to associate the detection of Leptospira spp. infection with clinicopathological and renal histopathological findings using a multidisciplinary approach. The present study isolated and characterized Leptospira spp. obtained from naturally infected dogs and described relevant clinical and histopathological findings. Blood and urine were collected from 57 dogs with clinical symptomatology suggestive of leptospirosis; 38 cases were confirmed by PCR in urine or by culture or microscopic agglutination testing (titers ≥800). A total of 12 strains of pathogenic Leptospira were isolated from the studied dogs (seven in blood, four in urine and one in both blood and urine samples). All isolates were characterized as Leptospira interrogans serogroup Icterohaemorrhagiae. Of the confirmed cases, almost one-third of the animals had been vaccinated. Our analysis of laboratory testing revealed that azotemia and proteinuria were statistically significant predictors of infection. The main histopathological findings seen in kidney tissues were necrosis, degeneration, tubular regeneration, mononuclear inflammatory infiltrate and congestion. A multidisciplinary approach involving clinicopathological and histopathological characterization of renal involvement can aid in the identification of acute leptospirosis infection.

Effect of diosmin on lipid peoxidation and organ damage against subacute deltamethrin exposure in rats.

The aim of this study was to investigate the protective efficacy of diosmin against subacute deltamethrin exposure. For this purpose, 40 male Wistar albino rats were used. The animals were assigned to the following 4 groups: control group (received corn oil vehicle alone), diosmin-treated group (50mg/kgbw/day orally), deltamethrin-exposed group (5mg/kgbw/day, orally) and coadministered group (5mg/kgbw/day deltamethrin and 50mg/kgbw/day diosmin, orally) for 28days. Some lipid peroxidation/antioxidant status/biochemical markers were evaluated in blood/tissue (liver, kidney, brain, heart and testis) samples and the histopathological architecture was assessed. Compared with the control group, no alteration was detected in the parameters and histological findings of the diosmin-treated group. Deltamethrin toxicity was associated with significantly increased plasma, cardiac, hepatic, renal, cerebral and testicular levels of MDA and NO, and significantly decreased GSH levels (p < 0.05). Antioxidant enzyme status (SOD, CAT and GSH-Px activities) displayed either decrease or increase (p < 0.05). Significant increase was detected in AST and ALT activities and urea and creatinine levels (p < 0.05). The values of the group coadministered with deltamethrin and diosmin were similar to the values of the control group. Diosmin ameliorated deltamethrin-induced lymphocytic and histiocytic infiltration and subendocardial oedema in the heart. Combined administration also minimized hepatic, renal, testicular and cerebral histopathological findings. The alterations detected in various toxicological parameters correlated well with the histopathological changes observed in various organs. In conclusion, it is suggested that diosmin could provide protection against deltamethrin-induced toxicity and organ damage in rats.

Renal Histopathological Post-Mortem Findings of 17 Patients with COVID-19 in New York City

Renal Histopathological Post-Mortem Findings of 17 Patients with COVID-19 in New York City

Lupus Nephritis diagnosed by stand-alone renal histopathological findings in a middle-aged male.

Systemic lupus erythematosus (SLE) is a systemic autoimmune condition, characterized by the production of autoantibodies, predominantly against nuclear antigens. It primarily affects women of childbearing age. Men account for 4-22% of all cases in various series (1,2). Lupus nephritis can be diagnosed with high sensitivity and specificity based on histopathological criteria alone (3). We report lupus nephritis in a 50-year-old male diagnosed solely on renal histopathological findings.

MON-202 EVALUATION OF SURROGATE PREDICTORS OF MORTALITY DUE TO SNAKE ENVENOMATION AND RENAL HISTOPATHOLOGICAL CORRELATION

To evaluate the surrogate predictors of mortality due to venomous snake bite and to study the spectrum of histopathological changes of kidney in death due to venomous snake bite. One year Descriptive, Observational, Cross-sectional, Hospital and Mortuary based study. During autopsy, detailed external and internal examination was done to find the macroscopic changes at the local area of bite, kidneys. The slices of tissue from Kidneys were taken from selected cases in such a way that a slice contains all the physiological layers of the organ including diseased and normal (as seen on naked eye examination) portions with intervening transitional zone. Stained slides were examined under microscope to identify any pathological changes in kidney tissues. The findings of histopathological study were compared with that of the normal tissues. Thus the pathological process as identified in respect to the tissue involved. Macroscopic features on autopsy shows 4.1% with only congestion, congested with focal medullary haemorrhage in 36.7%, congested with patchy corticomedullary haemorrhage in 8.2%, congested with diffuse haemorrhage in 51.02%. Renal histopathological findings shows the predominant feature is Tubular Necrosis found in 57.1% of cases. 8.2% of cases shows Cortical Necrosis. Thrombi in blood vessels were found in 14.3% of cases. Of the Tubular Necrosis cases 20.4% of cases presented with dilated tubules lined by flattened epithelium & tubules shows hyalinised material in its lumen; 8.2% of cases shows small tubules containing proteinetious material in their lumen. All the cases shows features of congestion and inflammation. Haemorrhage is seen in 95.9% of cases. The predominant feature is Tubular Necrosis found in 57.1% of cases. 8.2% of cases shows Cortical Necrosis. Thrombi in blood vessels were found in 14.3% of cases. Of the Tubular Necrosis cases 20.4% of cases presented with dilated tubules lined by flattened epithelium & tubules shows hyalinised material in its lumen; 8.2% of cases shows small tubules containing proteinetious material in their lumen. All the cases shows features of congestion and inflammation. Haemorrhage is seen in 95.9% of cases. Multivariate analysis shows only number of AVS (0.020), duration of hospital stay/period of survivability (0.024), bleeding manifestations (0.000), shock/hypotension (0.000) & DIC (0.000) are positively correlated with Tubular Necrosis. With Cortical Necrosis, there is correlation with DIC (0.026) only. Whereas, only shock/hypotension (0.013) gives positive correlation with the presence of thrombi in blood vessels The prognosis for snakebite depends on factors besides hospital treatment: whether first aid is given immediately after the bite, early initiation of appropriate treatment, and the type of snake involved along with amount and severity of venom. Histopathological changes, especially in renal tissue can aid in differentiating between the nature of snake and the damage it causes.

ARE PATIENTS WITH DIABETIC NEPHROPATHY DIFFERENT REGARDING RENAL ULTRASOUND PARAMETERS AND DOPPLER SONOGRAPHY FINDINGS COMPARED WITH RENAL HISTOPATHOLOGY?

Ultrasonography (US) findings and Doppler sonography of renal vessels can provide useful information on the structural and vascular supply of patients suffering from chronic kidney disease (CKD). The purpose of this study was to compare the US findings of patients with diabetic nephropathy with the pathologic findings of their renal biopsy. In this descriptive study, US parameters including resistivity index (RI), renal size and volume and cortical and medullary echogenicity, and histopathological findings of renal biopsy (fibrosis, inflammation and chronicity) of 60 patients (27 women and 33 men) with diabetic nephropathy admitted in Hasheminejad kidney center (HKC) of Tehran were extracted and analyzed. Of 60 patients, interstitial fibrosis (IF) in 47 patients, interstitial inflammation (II) in 50 patients and signs of chronicity in 43 patients in pathology report were observed. Patients with IF had larger renal length, higher sinus volume, coarse echogenicity, and abnormal medullary echogenicity, significantly. The presence of II was associated with larger renal length, higher renal and sinus volume, higher cortical echogenicity, and more patients with coarse echogenicity and abnormal medullary echogenicity. The observation of chronicity was significantly correlated with higher sinus volume and more patients with irregular renal rim. According to the findings of this study, renal length and volume, renal sinus volume, and the presence of coarse echogenicity and abnormal medullar echogenicity strongly correlate with renal histopathologic findings in patients with diabetic nephropathy. RI is not a suitable marker for identifying tubulointerstitial changes in these patients.

Dose and Exposure Time-Dependent Renal and Hepatic Effects of Intraperitoneally Administered Fumonisin B₁ in Rats.

Male Wistar rats were treated intraperitoneally (i.p.) with fumonisin B1 (FB1; 0, 20, 50 and 100 mg/kg dietary dose equivalent) for 5 and 10 days (n = 24–24 in each setting) to gain dose- and time-dependent effects on antioxidant status and oxidative stress response, clinical chemical endpoints and liver, kidney and lung histopathology and lymphocyte damage (genotoxicity). FB1 decreased feed intake, body weight gain and absolute liver weight, irrespective of the toxin dose. Relative kidney weight increased in the 10-day setting. Linear dose response was found for plasma aspartate aminotransferase, alanine aminotransferase, total cholesterol, urea and creatinine, and exposure time-dependence for plasma creatinine level. The latter was coupled with renal histopathological findings, tubular degeneration and necrosis and the detachment of tubular epithelial cells. The pronounced antioxidant response (reduced glutathione accretion, increasing glutathione peroxidase activity) referred to renal cortical response (5–10 days exposure at 50–100 ppm FB1). Hepatic alterations were moderate, referring to initial phase lipid peroxidation (exposure time dependent difference of conjugated diene and triene concentrations), and slight functional disturbance (↑ total cholesterol). Lymphocyte DNA damage was moderate, supporting a mild genotoxic effect of FB1.