Kidney Pathology Research Articles

What is the spectrum of kidney pathology associated with COVID-19?

Kidney involvement occurs in almost one third of patients hospitalised with coronavirus disease 2019 (COVID-19) and is associated with increased disease severity. This review aims to outline the spectrum of kidney pathology involved in COVID-19. Literature was reviewed systematically on the databases Medline OVID and Scopus in search of case reports, case series, cohort studies and autopsy studies of patients with COVID-19 who underwent kidney biopsies. Studies were published between August 2020 and November 2021. Fourteen studies consisting of 159 patients were included in this review. Acute tubular necrosis is the most common pathology followed by collapsing glomerulopathy, occurring in 40.1% and 28.9% of patients respectively. Of the 46 patients with collapsing glomerulopathy, 44 were of African descent with high-risk apolipoprotein L1 genotypes. Less common glomerular diseases include membranous nephropathy, secondary focal segmental glomerulosclerosis, minimal change disease and primary focal segmental glomerulosclerosis occurring in 5%, 4.4%, 3.1% and 2.5% of patients respectively. Glomerulonephritis occurred in a minority of patients. Direct viral infection has not been found as a definitive aetiology. Acute kidney injury occurs frequently in hospitalised COVID-19 patients and is associated with increased morbidity and mortality. The mechanisms underpinning acute kidney injury are multifactorial. Acute tubular necrosis is the most common. Collapsing glomerulopathy is the most common glomerular injury and is strongly linked to apolipoprotein L1 genotypes. Improved understanding of COVID-19-related kidney pathologies can guide treatment to improve patient outcomes and reduce progression of chronic kidney disease. The longitudinal impact of COVID-19-related kidney disease requires further research.

Association between perioperative platelet distribution width changes and postoperative acute kidney injury in patients with renal insufficiency: a retrospective study

BackgroundAcute kidney injury (AKI) is a major complication following cardiac surgery with a high incidence in those with existing kidney dysfunction. Platelet distribution width (PDW) reflects variability in platelet size and serves as an indicator of platelet activation. Recent investigations linked PDW changes to kidney pathology, suggesting its utility in identifying individuals at risk for AKI, thus necessitating exploration of its predictive value.MethodsPatients with preoperative renal dysfunction [15 ≤ estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73m2] who underwent cardiac surgery from January 2018 to December 2021 were retrospectively enrolled. PDW values were measured preoperatively and again upon admission to the ICU immediately after cardiac surgery, with the change in PDW (dPDW) defined as the difference between these two measurements. The primary outcome was postoperative AKI, defined base on the Kidney Disease: Improving Global Outcomes (KDIGO) definition and staging criteria. Multivariate regression models were performed to identify the association between dPDW and AKI and its potential trend. Restricted cubic spline analysis assessed non-linear associations between dPDW and AKI. The Youden index identified an optimal dPDW cut-off for AKI prediction. Subgroup analysis was performed to elucidate the consistency of these associations across the various subgroups.ResultsAKI occurred in 53.10% (513/966) of patients, accompanied by significant PDW increases in cases of AKI (P < 0.001). After adjusting confounders, dPDW was identified as a significant risk factor for AKI [odds ratio (OR) = 1.09, 95% confidence interval (CI): (1.02 ~ 1.16), P = 0.012]. Patients in the highest dPDW quartile (Q4) had a 195% higher AKI risk compared to those in the lowest quartile (Q1) (OR = 2.95, 95% CI:1.78 ∼ 4.90, P < 0.001). Trend analysis indicates that the risk of AKI increased with higher dPDW quartiles (P for trend < 0.001). Youden index showed that dRDW = 1.1 was identified as the optimal diagnostic cut-off value for AKI. Subgroup analyses and interaction tests showed a robust association between dPDW and AKI in all subgroups (P for interaction > 0.05).ConclusionsThis study underscored perioperative PDW changes as a significant predictor of postoperative AKI in patients with renal insufficiency, highlighting its potential in refining risk stratification and management strategies.Clinical trial numberNot applicable for this observational retrospective study.

Abnormalities in Hemostatic Parameters Related to Hemodialysis in End-stage Kidney Pathology: A Narrative Review

Abnormalities in Hemostatic Parameters Related to Hemodialysis in End-stage Kidney Pathology: A Narrative Review

The clinical efficacy of cGMP-specific sildenafil on mitochondrial biogenesis induction and renal damage in cats with acute on chronic kidney disease

BackgroundMitochondrial biogenesis (MB) induction has recently emerged as potential therapeutic approaches in kidney pathology and the mitochondria-targeted therapies should be investigated to improve treatment of animals with kidney diseases. This study aimed to investigate the effects of MB induction with sildenafil citrate on the cGMP/NO pathway, glomerular filtration, and reduction of kidney damage and fibrosis (TGF-β/SMAD pathway) in cats with acute on chronic kidney disease (ACKD). Thirty-three cats were divided into the non-azotemic (healthy) group (n:8) and the ACKD group (n:25), comprising different breeds, sexes, and ages. Sildenafil citrate was administered to the non-azotemic and ACKD groups (2.5 mg/kg, PO, q12 hours) for 30 days. Serum and urine NO, MDA, NGAL, KIM-1, TGF-β1, IL-18, FGF 23, PGC-1α and cGMP concentrations were measured.ResultsSerum cGMP concentrations increased (P < 0.05) in the non-azotemic group during the 2nd (median 475.99 pmol/mL) and 3rd (median 405.01 pmol/mL) weeks of the study, whereas serum cGMP concentrations decreased in the ACKD group during the 4th(median 188.52 pmol/mL) week compared to the non-azotemic group (P < 0.05). No difference was observed in serum biomarker concentrations except NO, which increased in the 4th week (P < 0.05). The urinary concentrations of NO, MDA, PGC-1α, TGF-β1, NGAL, KIM-1, IL-18, and FGF 23 in the ACKD group were found to be higher compared to those in the non-azotemic group from the 1st to the 4th week (P < 0.05). In the ACKD group, the urine PGC-1α concentration in the 2nd (median 6.10 ng/mL) week was lower compared to that in the 0 and 1st (median 7.65 and 7.21 ng/mL, respectively) week, and the NO concentration in the 3rd (median 28.94 µmol/mL) week was lower than that in the 0th (median 37.43 µmol/mL) week (P < 0.05).ConclusionsWhile sildenafil citrate has been determined to induce a low level of MB and to have a beneficial effect on glomerular filtration, it is observed to be ineffective in mitigating renal damage and fibrosis via the TGF-β/SMAD pathway in cats with ACKD.

Regulated cell death in chronic kidney disease: current evidence and future clinical perspectives

Chronic kidney disease (CKD) is the progressive loss of kidney function/structure over a period of at least 3 months. It is characterised histologically by the triad of cell loss, inflammation and fibrosis. This literature review focuses on the forms of cell death that trigger downstream inflammation and fibrosis, collectively called regulated cell death (RCD) pathways. Discrete forms of RCD have emerged as central mediators of CKD pathology. In particular, pathways of regulated necrosis – including mitochondrial permeability transition pore (mPTP)-mediated necrosis, necroptosis, ferroptosis and pyroptosis – have been shown to mediate kidney pathology directly or through the release of danger signals that trigger a pro-inflammatory response, further amplifying tissue injury in a cellular process called necroinflammation. Despite accumulating evidence in pre-clinical models, no clinical studies have yet targeted these RCD modes in human CKD. The review summarizes recent advances in our understanding of RCD pathways in CKD, looks at inter-relations between the pathways (with the emphasis on propagation of death signals) and the evidence for therapeutic targeting of molecules in the RCD pathways to prevent or treat CKD.

Взаємозв’язок між хронічною хворобою нирок та серцево-судинною патологією у хворих на цукровий діабет 2-го типу різного віку

The aim – to analyze the relationship between chronic kidney disease (CKD) and cardiovascular pathology in patients with type 2 diabetes (T2D) of different ages.Materials and methods. A total of 233 patients with T2D aged 30-80 years were examined. Anthropometric indicators, blood pressure, glucose levels, glycated hemoglobin, C-peptide, total cholesterol, triglycerides, low-density and high-density lipoprotein cholesterol, creatinine, glomerular filtration rate, AST, and ALT were measured in all patients. Groups of patients were compared based on the presence of CKD and age using Student’s t-test and Pearson’s chi-squared test.Results and discussion. In patients with T2D and CKD, the incidence of coronary heart disease (CHD) (OR 1.8; 95 % CI 1.02–3.23; p=0.044), myocardial infarction (OR 2.0; 95 % CI 1.01–3.95; p=0.046), and strokes (OR 2.66; 95 % CI 1.07–6.63; p=0.036) is significantly higher compared to patients with T2D without kidney pathology. When comparing the clinical indicators of patients with T2D combined with CKD and those without it, no significant differences were found in anthropometric measurements, blood pressure, blood glucose levels, glycated hemoglobin, or C-peptide levels. The levels of total cholesterol, hemoglobin, and red blood cell count in the blood were significantly lower (р&lt;0.05), while the levels of creatinine and glomerular filtration rate were significantly higher (р&lt;0.001) in patients with kidney pathology.Conclusion. In patients with T2D, a relationship between CKD and cardiovascular pathology has been established. It can be assumed that the development of kidney pathology in patients with T2D is a significant risk factor for cardiovascular diseases.

Cloperastine Reduces IL-6 Expression via Akt/GSK3/Nrf2 Signaling in Monocytes/Macrophages and Ameliorates Symptoms in a Mouse Sepsis Model Induced by Lipopolysaccharide.

Cloperastine (CLP) is a drug with a central antitussive effect that is used to treat bronchitis. Therefore, we have attempted to examine the anti-inflammatory effects of CLP. CLP reduced the secretion of interleukin (IL)-6, a pro-inflammatory cytokine, from RAW264.7 monocyte/macrophage-linage cells treated with lipopolysaccharide (LPS). IL-6 is a biomarker of sepsis and has been suggested to exacerbate its symptoms. We found that the intraperitoneal administration of CLP reduced IL-6 levels in the lungs and also improved hypothermia in mice with LPS-induced sepsis. CLP ameliorated kidney pathologies such as congestion and increased the survival rate of mice administered with a lethal dose of LPS. To reveal the mechanisms underlying the anti-inflammatory function of CLP, we analysed the intracellular signaling in LPS-treated RAW264.7 cells. CLP induced the phosphorylation of protein kinase B (Akt) and glycogen synthase kinase 3 (GSK3) and also increased the amount of nuclear factor erythroid-2-related factor 2 (Nrf2) in RAW264.7 cells with/without LPS. Wortmannin, an inhibitor of phosphoinositide 3-kinase (PI3K), reduced the upregulated phosphorylation levels of Akt and GSK3 and the increased amount of Nrf2. It also halted the reduction of IL-6 secretion caused by CLP. These results suggest that CLP has an anti-inflammatory function via Akt/GSK3/Nrf2 signaling and could be a candidate drug for the treatment of inflammatory diseases, including sepsis.

Phosphorus restriction prevents rapamycin-induced kidney damage in rats.

There are conflicting reports about the effect or rapamycin on the kidneys. Rapamycin is known to promote phosphaturia that may be associated to renal injury. Detailed histopathological studies were performed on the kidneys of rats with normal (Control) and reduced (Nx) renal mass that were treated with rapamycin (1.3 mg/kg for 22 days) or placebo. The effect of rapamycin was also evaluated in Control and Nx rats fed different amounts of phosphorus: 0.6% P (NP), 1.2% P (HP) and 0.2% P (LP). Quantitative scores of kidney lesions were obtained for: interstitial nephritis (IN), tubular damage (TD), and nephrocalcinosis (NC). When compared with placebo, rapamycin administration to Nx rats resulted in significant increases in IN (4.17±0.74 vs 1.51±0.53 %) and TD (14.45±1.51 vs 8.61±1.83 %). Rapamycin also increased NC both in Control (0.86±0.23 vs 0.14±0.06 %) and Nx (0.86±0.32 vs 0.15±0.14 %) rats. In Control rats receiving rapamycin, feeding HP aggravated IN (3.25±0.48 %), TD (22.47±4.56 %) and NC (3.66±0.75 %) while feeding LP prevented development of any renal lesions. In Nx rats treated with rapamycin, HP intake also increased IN (8.95±1.94 %), TD (26.86±3.95 %) and NC (2.77±0.60 %) whereas feeding LP reduced all lesions to lower levels than in rats fed NP. Rapamycin treatment increased fractional excretion of P (FEP) and an excellent correlation between scores for renal lesions and FEP was found. Rapamycin has deleterious effects on kidney pathology causing lesions that are located mainly at tubular and tubulo-interstitial level. Rapamycin-induced kidney damage is more evident in rats that already have decreased renal function and seems to be related to the phosphaturic effect of the drug. Dietary P restriction prevents kidney damage in rats treated with rapamycin.

Self-Supervised Learning for Feature Extraction from Glomerular Images and Disease Classification with Minimal Annotations.

Deep learning has great potential in digital kidney pathology. However, its effectiveness depends heavily on the availability of extensively labeled datasets, which are often limited due to the specialized knowledge and time required for their creation. This limitation hinders the widespread application of deep learning for the analysis of kidney biopsy images. We applied self-distillation with no labels (DINO), a self-supervised learning method, to a dataset of 10,423 glomerular images obtained from 384 PAS-stained kidney biopsy slides. Glomerular features extracted from the DINO-pretrained backbone were visualized using principal component analysis (PCA). We then performed classification tasks by adding either k-nearest neighbor (kNN) classifiers or linear head layers to the DINO-pretrained or ImageNet-pretrained backbones. These models were trained on our labeled classification dataset. Performance was evaluated using metrics such as the area under the receiver operating characteristic curve (ROC-AUC). The classification tasks encompassed four disease categories (minimal change disease, mesangial proliferative glomerulonephritis, membranous nephropathy, and diabetic nephropathy) as well as clinical parameters such as hypertension, proteinuria, and hematuria. PCA visualization revealed distinct principal components corresponding to different glomerular structures, demonstrating the capability of the DINO-pretrained backbone to capture morphological features. In disease classification, the DINO-pretrained transferred model (ROC-AUC = 0.93) outperformed the ImageNet-pretrained fine-tuned model (ROC-AUC = 0.89). When the labeled data were limited, the ImageNet-pretrained fine-tuned model's ROC-AUC dropped to 0.76 (95% confidence interval [CI], 0.72-0.80), whereas the DINO-pretrained transferred model maintained superior performance (ROC-AUC 0.88, 95% CI 0.86-0.90). The DINO-pretrained transferred model also exhibited higher AUCs for the classification of several clinical parameters. External validation using two independent datasets confirmed DINO pre-training's superiority, particularly when labeled data were limited. The application of DINO to unlabeled PAS-stained glomerular images facilitated the extraction of histological features that can be effectively utilized for disease classification.

Matrix metalloproteinases in kidney homeostasis and diseases: an update.

Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases with important roles in kidney homeostasis and pathology. While capable of collectively degrading each component of the extracellular matrix, MMPs also degrade nonmatrix substrates to regulate inflammation, epithelial plasticity, proliferation, apoptosis, and angiogenesis. More recently, intriguing mechanisms that directly alter podocyte biology have been described. There is now irrefutable evidence for MMP dysregulation in many types of kidney disease including acute kidney injury, diabetic and hypertensive nephropathy, polycystic kidney disease and Alport syndrome. This updated review will detail the complex biology of MMPs in kidney disease.

Characteristics of risk factors and molecular genetic parameters in children with chronic kidney disease

Introduction. Information about the health status of children with nephrological pathology includes many manifestations of functional system disorders. However, early diagnosis of chronic kidney disease (CKD) is rarely carried out due to the lack of reliable predictors of this process.The aim: To analyze the association of anamnestic signs, laboratory and genetic research results with chronic kidney disease in children to identify potential predictors of the disease.Material and Methods. The data were obtained from a single-center retrospective catamnestic cohort study (2011–2022). The main group included 128 children with chronic kidney disease aged 1 to 17 years. The comparison group consisted of 30 children without diagnosed kidney pathology aged from 1 to 17 years. There were no statistically significant differences in sex and age between the two groups. The informative value of more than 150 features, including anamnestic ones, the state of the mother’s health during pregnancy, antenatal and perinatal factors, features of the child’s development and manifestation of the disease, the results of clinical, laboratory, and genetic research methods were evaluated. An integrated approach to the study included methods for hypotheses testing on statistical significance of indicators differences, regression analysis, and ROC analysis.Results. Hereditary burden of nephrological pathology in the family, unfavorable course of pregnancy (anemia, toxicosis of the first half), obstetric and somatic pathology in the mother, the serial number of childbirth are associated with the subsequent development of CKD. Erythrocytes in the urine and daily protein loss were detected only in the group of children with CKD. In this group, a decrease in the number of red blood cells, increased erythrocyte sedimentation rate (ESR), allergies at an early age, otitis media, persistent viral and bacterial infections, and a number of signs of connective tissue dysplasia were more common. The main group statistically significantly differed from the comparison group by a number of polymorphic genetic markers. It can be assumed that the polymorphisms AGT1 Thr174Thr, AGT2 Thr235Thr, NO3 C786T are associated with a predisposition to CKD, and the products of polymorphisms AGT1 Thr174Met, AGT2 Met235Met, R1 AGT2 C1166C, NO3 T786T may have a protective effect according to development of CKD.Conclusion. The risk factors for CKD identified in this study can be used to develop software to support medical decision making for early detection of children at high risk of disease progression.

Comprehensive evaluation of the nephrotoxicity of carbon quantum dots: Effects of the surface charge

Carbon quantum dots (CQDs) are garnering attention for their broad applications. This study offers a detailed evaluation of the biomedical safety and health risks of carbon quantum dots (CQDs) with different surface modifications, addressing a key gap in their safe application. It focuses on three CQD types: diammonium citrate-based (CQDs-A), spermidine trihydrochloride-based (CQDs-S), and a combination (CQDs-A/S), analyzing their physicochemical properties, cytotoxicity, oxidative stress, inflammatory responses, and nephrotoxicity. While all CQDs were under 10 nm, their biological impacts varied. Positively charged CQDs-S and CQDs-A/S showed significant cytotoxicity in HEK293 cells, inducing oxidative stress but not activating NLRP3 inflammasome, indicating a limited inflammatory response. Renal integrity remained unaffected, with stable zonula occludens 2 expression and unaltered renal markers. In vivo studies in BALB/c mice further supported the safety of CQDs, showing no organ damage or kidney pathology at high doses. The findings underscore the potential for safe biomedical use of CQDs, particularly when their retention time is minimized. This research makes a novel contribution by linking CQDs' surface charge to cytotoxic effects and oxidative stress, providing key insights into their safe use in biomedicine and filling a critical gap in nanoparticle toxicity studies.

Association of Urinary Adhesion Molecules Derived from Endothelial Cells and Kidney Pathology in ANCA-Associated Glomerulonephritis

Association of Urinary Adhesion Molecules Derived from Endothelial Cells and Kidney Pathology in ANCA-Associated Glomerulonephritis

Spectrum of Kidney Pathology in Patients with Syphilis

Spectrum of Kidney Pathology in Patients with Syphilis

Development, Implementation, and Assessment of an Innovative Kidney Pathology Curriculum

Development, Implementation, and Assessment of an Innovative Kidney Pathology Curriculum

Dual-antigen fusion protein vaccination induces protective immunity against Candida albicans infection in mice

ABSTRACT Candida albicans Is a leading cause of nosocomial bloodstream infections, particularly in immunocompromised patients. Current therapeutic strategies are insufficient, highlighting the need for effective vaccines. This study aimed to evaluate the efficacy of a dual-antigen fusion protein vaccine (AH) targeting the Als3 and Hyr1 proteins of C. albicans, using AlPO4 as an adjuvant. The AH vaccine was constructed by fusing Als317-432 and Hyr125-350 proteins, and its immunogenicity was tested in BALB/c mice and New Zealand white rabbits. Mice received three intramuscular doses of the vaccine combined with AlPO4, followed by a lethal challenge with C. albicans SC5314. Survival rates, antibody responses, cytokine production, fungal burdens, and organ pathology were assessed. The vaccine’s efficacy was also validated using rabbit serum. Mice vaccinated with the AH-AlPO4 combination exhibited significantly higher antibody titers, particularly IgG and its subclasses, compared to controls (p < .001). The survival rate of vaccinated mice was 80% post-infection, significantly higher than the control group (p < .01). Vaccinated mice showed reduced fungal loads in the blood, kidneys, spleen, and liver (p < .05). Increased levels of interferon gamma and interleukin (IL)-17A were observed, indicating robust T helper (Th) 1 and Th17 cell responses. Vaccination mitigated organ damage, with kidney and liver pathology scores significantly lower than those of unvaccinated mice (p < .05). Rabbit serum with polyclonal antibodies demonstrated effective antifungal activity, confirming vaccine efficacy across species. The AH-AlPO4 vaccine effectively induced strong immune responses, reduced fungal burden, and protected against organ pathology in C. albicans infections. These findings support further development of dual-antigen vaccine strategies.

Разработка интеллектуальной системы поддержки принятия врачебных решений для прогнозирования хронической болезни почек у детей.

Introduction. Chronic kidney disease is often diagnosed too late. Currently, the diagnostic accuracy is 44.1%, which highlights the urgent need to improve diagnostic methods. The purpose of the study: to develop a model – a system of support of medical decisions to predict chronic kidney disease in children. Materials and methods. А one-center retrospective cohort study (2011–2022) of children with chronic kidney disease of 1–4 stages in the age from 1 to 17 years. To construct a predictive model for diagnosing chronic kidney disease in children, an ensemble learning method was used, using which the models obtained by machine learning algorithms were combined: multi-factor logistic regression and decision tree. The models use five variables: asthenic physique in a child, loss of protein and red blood cells with urine, ESR and blood serum sodium. Results. The study involved 158 patients. The main group includes 128 children with chronic kidney disease of stage 1–4 aged 1–17. The comparison group was 30 children with no diagnosed kidney pathology aged 1 to 17. The children of the two groups did not differ statistically by sex and age. A model has been obtained to predict chronic kidney disease in children on a test sample with an accuracy of 93.5% [87.1; 100.0]%; a sensitivity of 92.0% [82.1; 100.0]; a specificity of 100.0% [100.0; 100.0.0]; ROC-AUC = 98.7%;100.0].0. Obtained model of excellent quality (&gt;90%). The model describes 90.3% [83.8; 96.1]% variance. Conclusion. The proposed model demonstrates excellent predictive ability and may be of important clinical importance for predicting the chronic process in primary health care, where symptoms associated with the risk of chronic kidney disease, may be overlooked. Predicting and developing early nephroprotective strategies can lead to better treatment outcomes and prolong life.

How much salt should i recommend to a patient with CKD: the real mechanisms of regulation of sodium metabolism in kidney pathology

How much salt should i recommend to a patient with CKD: the real mechanisms of regulation of sodium metabolism in kidney pathology

Tissue Kallikrein-1 Suppresses Type I Interferon Responses and Reduces Depressive-Like Behavior in the MRL/lpr Lupus-Prone Mouse Model.

Excessive production and response to Type I interferons (IFNs) is a hallmark of systemic lupus erythematosus (SLE). Neuropsychiatric lupus (NPSLE) is a common manifestation of human SLE, with major depression as the most common presentation. Clinical studies have demonstrated that IFNα can cause depressive symptoms. We have shown that the kallikrein-kinin system (KKS) [comprised of kallikreins (Klks) and bradykinins] and angiotensin-converting enzyme inhibitors suppressed Type I IFN responses in dendritic cells from lupus-prone mice and human peripheral blood mononuclear cells. Tissue Klk genes are decreased in patients with lupus, and giving exogenous Klk1 ameliorated kidney pathology in mice. We retro-orbitally administered mouse klk1 gene-carrying adenovirus in the Murphy Roths Large lymphoproliferative (MRL/lpr) lupus-prone mice at early disease onset and analyzed immune responses and depressive-like behavior. Klk1 improved depressive-like behavior, suppressed interferon-responsive genes and neuroinflammation, and reduced plasma IFNα levels and proinflammatory cytokines. Klk1 also reduced IFNAR1 and JAK1 protein expression, important upstream molecules in Type I IFN signaling. Klk1 reduced bradykinin B1 receptor expression, which is known to induce proinflammatory response. Together, these findings suggest that Klk1 may be a potential therapeutic candidate to control IFNα production/responses and other inflammatory responses in SLE and NPSLE.

Clinical and pathological renal outcomes of COVID-19 patients: an Egyptian retrospective multi-center pooled analysis

BackgroundKidneys have been one of the different organs affected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) since its discovery, Acute kidney injury was the most common presentation. A pooled data from different kidney centers or hospitals in Egypt who sent their renal biopsy specimens from patients with renal trouble, up to 4 months after catching SARS-CoV-2, to PATH LAB for diagnosis, were analyzed.ResultsBeside acute kidney injury, a variety of different presentations was found, such as accidentally discovered impaired kidney function, varying degrees of proteinuria, and nephrotic syndrome. Not only acute tubular injury, acute tubulointerstitial nephritis, or thrombotic microangiopathy, but the extent of observation for 4 months revealed, unexpected pathologies, such as podocytopathies, membranous glomerulonephritis, proliferative and necrotizing glomerulonephritis, and lupus nephritis.ConclusionThis virus has been incriminated in a chain of different kidney disease presentations and pathologies, although, a causal relationship is difficult to prove.