Glomerular Hematuria Research Articles

Diagnosis and Treatment of Hematuria

Hematuria is a common manifestation caused by various factors such as infection, inflammation, trauma, urinary stone and malignancy. Hematuria reflects pathological state of urinary system. Isolated microscopic hematuria without any abnormalities besides of hematuria on urine microscopic examination usually presents a good clinical course or outcome. However, significant proteinuria or hypertension, which accelerates renal dysfunction, can often develop during follow-up period in patients with isolated microscopic hematuria. Compared with non-glomerular hematuria, glomerular hematuria shows several characteristic findings such as dysmorphic red blood cell (RBC) or RBC casts or significant proteinuria on urinalysis. If glomerular hematuria is strongly suspected, a kidney biopsy may be required to differentiate the cause of glomerulonephritis. In this review, we tried to review the differential diagnosis and diagnostic approach and treatment of hematuria.

Glomerular Hematuria as a Predictor of Renal Prognosis in Malignant Hypertension Patients with Thrombotic Microangiopathy: A Propensity Score-Matched Analysis of a Biopsy-Based Cohort Study

Introduction: Malignant hypertension (mHTN) is a hypertensive emergency. Thrombotic microangiopathy (TMA) is a widespread complication of mHTN. Few studies have evaluated whether glomerular hematuria provides prognostic information for renal dysfunction in patients with mHTN-associated TMA. Methods: This observational cohort study included 292 patients with mHTN-associated TMA based on renal biopsy. Propensity-score matching (PSM) analysis was conducted to adjust for clinical characteristics in a comparison between with and without glomerular hematuria. Cox regression was employed to identify risk factors for renal prognosis. Results: A total of 70 patients with glomerular hematuria were compared to 222 patients with non-glomerular hematuria. After PSM, 67 pairs of patients with mHTN-associated TMA were matched. Patients with glomerular hematuria exhibited lower serum albumin levels, higher 24-h proteinuria, and a higher prevalence of glomerular sclerosis than those with non-glomerular hematuria. Glomerular hematuria was independently associated with deteriorated renal function compared with non-glomerular hematuria (HR: 0.51; 95% CI: 0.29–0.89, p = 0.019). This association remained significant after PSM (HR: 0.51; 95% CI: 0.28–0.91, p = 0.022). Additionally, glomerular hematuria was independently associated with renal replacement therapy (RRT) (HR: 3.14; 95% CI: 2.06–5.66, p < 0.001). This difference remained significant after PSM comparison (HR: 2.41; 95% CI: 1.34–4.33, p = 0.003). Furthermore, despite intensive blood pressure control, patients with glomerular hematuria experienced a higher incidence of RRT and a poorer recovery in renal function, specifically a 25% reduction of creatinine levels, compared to patients with non-glomerular hematuria. Conclusion: Glomerular hematuria is significantly associated with an increased risk of adverse renal outcomes in patients with mHTN-associated TMA.

#2182 An unexpected life-threatening cause of kidney failure

Abstract Background and Aims Kidney failure can appear in acute clinical conditions and the cause cannot always be determined, as in approximately 40% of cases that require renal replacement therapy (RRT). In addition, there are other cases in which a patient with persistently low estimated glomerular filtration rate (eGFR) for 3 months is treated with RRT without a primary renal diagnosis. Systemic sclerosis (SSc) is a rare condition that can lead to RRT due to renal ”crisis”. Autopsy studies reveal kidney pathology in approximately 60 percent of patients with SSc. In addition, as many as 50 percent of patients with SSc have markers of kidney disease, as manifested by mild proteinuria, elevated serum creatinine concentration, and/or hypertension. The aim of our paper is to describe a case in which hemodialysis was initiated in emergency setting and the diagnosis was established after that. However clinical course was fatal and the final diagnosis was SSc. Method A 65-year-old male patient was admitted to the Nephrology department with a weight loss of 20 kg in 2 years, depression, low appetite and progressive decline of physical strength. He was previously diagnosed with diabetes mellitus (DM) and high blood pressure (HBP), the ponderal loss being attributed to DM. Insulin treatment was initiated together with antihypertensive medication. In the following 3 months, the kidney function deteriorated progressively and hemodialysis was started. Gray scale and CEUS US were performed to assess a possible cause of kidney failure. However, after the commencement of hemodialysis, the clinical condition did not improve and patient died in respiratory failure complicated by continuous pleural effusion. A skin biopsy from the right thigh was performed for the positive diagnosis. Results At clinical evaluation the patient was cachectic, with striking generalized parchment-like skin lesions which were suggestive both for ichthyosis or SSc. Laboratory tests revealed hyperglycemia, anemia, hypoalbuminemia, increased lactate dehydrogenase and creatine kinase (CK), mild proteinuria and glomerular hematuria. On the other side, myositis antibodies (AB) panel, antinuclear AB, tumor markers for pancreas and gastro-intestinal carcinoma, AB for vasculitis and lupus were negative. Ultrasound (US) (grey scale and CEUS) described dilated bile ducts and gallbladder with massive sludge, without evidence of tumoral neovascularization, and shrunk kidneys with hypoechoic medulla. CT scan confirmed the US findings. Dialysis parameters indicated kt/V 1.4 and urea reduction ratio of 79%. Therefore, no metabolic disturbances could explain the severely altered medical status. The clinical condition of the patient made the kidney biopsy unfeasible. Nevertheless, we decided to perform a skin biopsy, which revealed gross collagen bands, absence of sebaceous glands or hair follicles, as well as rare capillaries with lymphocyte inflammatory infiltrate and absence of hypoderma, thus confirming the diagnosis of SSc. Conclusion SSc can present with obscure clinical signs, leading to multiple organ dysfunction and initially unapparent cause of kidney failure. However, clinicians must be aware of potentially suggestive etiological signs such as parchment-like skin lesions and high blood pressure in a patient with multiple comorbidities. One must differentiate a dehydrated skin from a pathognomonic skin lesion as it is in SSc.

#2984 SLE associated fibrillary glomerulonephritis vs SLE nephritis with fibrils: can a straightforward distinction always be made?

Abstract Background and Aims Fibrillary glomerulonephritis (FGN) is an uncommon but serious kidney disease with unclear aetiology, variable prognosis, and a not well-established treatment. FGN has been associated with autoimmune diseases including SLE. Other aetiologies comprise diabetes, malignancies, HCV and chronic infections. Our goal is to discuss the pathologic and clinical differential diagnosis conundrums that a patient with a suspected SLE presented. Method We present the case of a 53-year-old woman evaluated for proteinuria (1 g/24 h), and glomerular haematuria. Renal function was normal. She referred mild arthralgias for the past two years. Her medical history was unremarkable for diabetes and hypertension. ANA and anti-dsDNA were positive. The rest of the immunological work-up was normal as well as protein immunofixation/free light chains. HCV, HBV, and HIV serology was negative. A thorough evaluation for malignancy was negative. A renal biopsy was performed. Results The renal biopsy showed enlarged glomeruli with mesangial matrix expansion (Congo-red negative), mild mesangial hypercellularity and focal endocapillary hypercellularity without hyaline deposits, fibrinoid necrosis or crescents, without significant chronic lesions (Fig. 1). A probable diagnosis based on light microscope could be that of a lupus nephritis class III with low activity and low chronicity indices. Immunofluorescence demonstrated weak or moderate immunofixation of IgG (2+), IgA(1+), C3(2+), C1q(1+), κ(1+) and λ(1+) in the mesangium and segmentally in the capillary walls with a smudgy appearance. IgM, C4, fibrinogen and albumin were negative. The lack of a full-house pattern and, more significantly, the low C1q intensity raised some questions about the validity of a lupus nephritis diagnosis. Ultrastructural evaluation revealed abundant fibrils that occupied the mesangium and permeated the glomerular basement membranes (GBMs). Fibrils were non branching and randomly oriented with a mean diameter of ∼15 nm (range: 11,87 nm -18,84 nm) (Fig. 2). No electron dense deposits, fingerprint deposits or tubuloreticular inclusions were detected. Immunohistochemical staining for DNA-J heat-shock protein family member B9 (DNAJB9) was then performed showing strong positivity in the mesangial matrix and GBMs. Interestingly, C4d was also strongly positive with the same pattern as DNAJB9. The diagnosis of fibrillary glomerulonephritis was suggested, mostly based on ultrastructural evaluation and immunohistochemical findings. Conclusion It is well known that the characteristic features of lupus nephritis (intense C1q staining, full-house staining, extraglomerular deposits, tubuloreticular inclusions, and combined subendothelial and subepithelial deposits) are, in some cases, neither universally present nor specific for lupus nephritis. Of special interest is the identification of fibrils in the renal biopsy of an SLE patient. The crucial importance of distinguishing between SLE associated FGN and SLE nephritis with fibrils is based on the generally poor renal prognosis of FGN as well as the unsatisfactory performance of immunosuppression. The differential diagnosis can be very challenging especially when DNAJB9 is not available.

Kidney Measurement and Glomerular Filtration Rate Evolution in Children with Polycystic Kidney Disease.

Autosomal dominant polycystic kidney disease (ADPKD) is an inherited disorder characterized by renal tubular cystic dilatations. The cysts can develop anywhere along the nephron, and over time the cystic dilatation leads to kidney enlargement. On the other hand, the cysts begin to reduce the number of functional nephrons as a consequence of cystic expansion that further contributes to the decline in renal function over the years. The pressure exerted by the dilated cysts leads to compensatory mechanisms that further contribute to the decline in renal function. These structural changes are responsible of glomerular hyperfiltration states, albuminuria, proteinuria, and hematuria. However, the presentation of ADPKD varies in children, from a completely asymptomatic child with incidental ultrasound detection of cysts to a rapidly progressive disease. There have been reports of early onset ADPKD in children younger than 2 years that showed a more rapid decline in renal function. ADPKD is caused by a mutation in PKD1 and PKD2 genes. Today, the PKD1 gene mutation seems to account for up to 85% of the cases worldwide, and it is associated with worse renal outcomes. Individuals with PKD2 gene mutation seem to present a milder form of the disease, with a more delayed onset of end-stage kidney disease. The cardinal sign of ADPKD is the presence of renal cysts during renal ultrasound. The current guidelines provide clinicians the recommendations for genetic testing in children with a positive family history. Given that the vast majority of children with ADPKD present with normal or supra-normal kidney function, we explored the glomerular filtration rates dynamics and the renal ultrasound-adjusted percentiles. In total, 14 out of 16 patients had kidney percentiles over 90%. The gene mutations were equally distributed among our cohort. In addition, we compared the modified Schwartz formula to the quadratic equation after adjusting the serum creatinine measurements. It seems that even though children with ADPKD have enlarged kidneys, the renal function is more likely normal or near normal when the quadratic estimation of glomerular filtration rate is used (qGFR tended to be lower, 111.95 ± 12.43 mL/min/1.73 m2 when compared to Schwartz eGFR 126.28 ± 33.07 mL/min/1.73 m2, p = 0.14). Also, when the quadratic equation was employed, not even a single patient reached the glomerular hyperfiltration threshold. The quadratic formula showed that glomerular filtration rates are linear or slightly decreasing after 1 year of follow-up (quadratic ΔeGFR = -0.32 ± 5.78 mL/min/1.73 m2), as opposed to the Schwartz formula that can falsely classify children in a hyperfiltration state (ΔeGFR = 7.51 ± 19.46 mL/min/1.73 m2), p = 0.019.

Slowly Progressive ANCA-associated Glomerulonephritis with Strong Mesangial MPO Deposits Following a Diagnosis of Interstitial Lung Disease.

An elderly woman showed positive conversion of myeloperoxidase (MPO)-antineutrophil cytoplasmic antibodies (ANCAs) following the diagnosis of interstitial lung disease (ILD) and glomerular hematuria and subsequently experienced slowly progressive glomerulonephritis. A kidney biopsy revealed chronic damage and necrotizing crescentic glomerulonephritis with mesangial MPO deposits. After corticosteroid treatment, the patient's urinalysis results and MPO-ANCA titers almost normalized and her renal function stabilized. This case is similar to recently reported cases of slowly progressive ANCA-associated glomerulonephritis. ILD likely triggered the production of MPO-ANCAs, and the accumulation of MPO deposits in the glomeruli may have contributed to the progression of her renal disease.

Detection of glomerular hematuria through an incidental finding in urinary sediment

Detection of glomerular hematuria through an incidental finding in urinary sediment

The relationship between immun staining and progression markers in IgA nephropathy

Objective: To determine the relationship between immunofluorescence microscopy findings and progression markers at the time of diagnosis in immunoglobulin A (IgA) nephropathy. Methods: Fifty-two patients with pathological diagnosis of primary IgA nephropathy by showing mesangial and mesangiocapillary IgA-dominant immune deposits in immunofluorescence microscopy were included in the study. At the time of biopsy, biochemical and hematological data, Oxford MEST score and immunofluorescent staining findings were recorded. The serum IgA/C3 ratio was calculated. The immunofluorescence results of the total group were compared with the markers of progression at the time of diagnosis, estimated glomerular filtration rate (eGFR), hematuria, proteinuria, creatinine, and serum IgA/C3 ratio. Results: The mean age of the study group was 39.9±12.3 years and 55.8% were male. eGFR, albumin, hemoglobin, IgM were significantly lower, and uric acid and hematuria were significantly higher in those with proteinuria above 1 g compared to those with low proteinuria. A positive correlation was found between IgA, C3 and lambda staining and hematuria. There was a positive correlation between C3 staining and creatinine, and a positive correlation with hematuria. A correlation was found between Kappa staining and eGFR. Conclusion: Correlation was found between IgA, C3 and lambda staining and hematuria at the time of diagnosis in IgA nephropathy.

Safety and effectiveness of COVID-19 vaccines in patients with IgA nephropathy: a retrospective cohort study from the TriNetX global collaborative networks

This study aimed to evaluate the renal safety and effectiveness of COVID-19 vaccination in patients with immunoglobulin A nephropathy (IgAN). We conducted a global and retrospective collaborative network analysis using TriNetX data from September 11, 2018 to September 11, 2023, to address this question. The study recorded diagnoses of IgAN, COVID-19 vaccinations, and outcomes of effectiveness using International Classification of Diseases, Tenth Revision, Clinical Modification codes and procedure codes. Propensity score matching (PSM) created matched groups (1:1). Hazard ratios (HR) with 95% confidence intervals (95% CI) were calculated for outcomes of effectiveness, and Kaplan-Meier method assessed survival probability. Safety outcomes regarding renal function were compared with estimated glomerular filtration rate (eGFR), proteinuria, and hematuria. Subgroup analyses were based on sex and age group. Sensitivity analysis was done before the outbreak of Omicron (from September 11, 2018 to October 31, 2021). The study involved 1010 vaccinated and 2776 unvaccinated patients with IgAN without COVID-19 infection at baseline. After PSM (1:1) with 25 variables, both groups consisted of well-matched 979 patients who were relatively young (around 55 years old) and in good health (eGFR: 78-80ml/min/1.732m2). Compared to the non-vaccinated group, vaccinated patients had significantly lower risks of COVID-19 infection and complications, including COVID-19 infection (HR: 0.050, 95% CI: 0.026, 0.093), COVID-19 pneumonia (HR: 0), severe lung complication (0.647, 95% CI: 0.421, 0.994), acute respiratory failure (0.625, 95% CI: 0.400, 0.978), sepsis (0.545, 95% CI: 0.334, 0.890), emergency department visits (0.716, 95% CI: 0.615, 0.833), all hospitalizations (0.573, 95% CI: 0.459, 0.715), and mortality (0.595, 95% CI: 0.366, 0.969). However, one month after the follow-up, the vaccinated group exhibited a slightly, but statistically significantly, lower eGFR compared to the non-vaccinated group (73.58 vs. 83.05ml/min/1.732m2, p=0.047). Nine months after the follow-up, the difference in eGFR between the two groups disappeared. The lower risk of COVID-19 infection was observed across genders (male and female) and age groups (young and old). For the period before Omicron outbreak, results were also similar. In the largest TriNetX matched cohort study of IgAN, COVID-19 vaccination was associated with a reduced risk of COVID-19 infection and associated complications. However, careful monitoring of renal function, especially GFR, is advisable. This study was supported by grant TCVGH-1103602C, TCVGH-1103601D, and TCVGH-1113602D from Taichung Veterans General Hospital.

Clinical and histopathological study of glomerular diseases in children

ABSTRACT Objective: To investigate the histopathological and clinical pattern of glomerular diseases in children. Method: A cross - sectional descriptive study was conducted on 71 children with glomerular disease who underwent kidney biopsy from January 2020 to December 2022. Results: Pure nephrotic syndrome was the main diagnosis before kidney biopsy (59.3%), followed by non - pure nephrotic syndrome with 12.7%, Schonlein Henoch nephritis, Lupus nephritis, IgA nephropathy, accounting for 11.2%, 8.4%, 5.6%, respectively. Hemolytic uremic syndrome and Alport syndrome accounted for 1.4% of each type. After being diagnosed by histopathological results, minimal change disease was most common with 36.6% in the primary group, and Lupus nephritis was found mainly with 15.5% in the secondary group. Among the clinical manifestations of glomerular diseases, hematuria, and extrarenal manifestations were significantly different among the glomerular groups (p &lt; 0.05). The ratio of change in diagnosis after the renal biopsy was 38%, in which IgA nephropathy had the lowest ratio, and Lupus nephritis and nephrotic syndrome had the highest ratio. Conclusions: Minimal change disease predominated in the group of primary glomerular disease, and Lupus nephritis was the majority in the group of secondary glomerulonephritis. Hematuria and extrarenal manifestations were clinically significant differences among groups of glomerular diseases.

#5201 KIDNEY BIOPSY IN PATIENTS WITH TYPE 2 DIABETES: A SINGLE CENTER OBSERVATIONAL STUDY

Abstract Background and Aims Patients with type 2 diabetes mellitus (T2DM), may have various underlying causes contributing to kidney disease beyond diabetic nephropathy (DN). In such cases, a kidney biopsy (KB) can provide a definite diagnosis and allow for tailored treatment options. The aim of this study is to evaluate non diabetic kidney disease (NDKD) in T2DM patients and identify data to support KB indications. Method This is a retrospective observational study that included patients with T2DM who were submitted to a native KB between 2011 and 2022. We collected demographic, clinical and laboratory data at the date of biopsy. KB indication was considered in order to include the patients in the first encountered criteria defined sequentially as the presence of (1) nephrotic syndrome, (2) low or rapidly declining estimated glomerular filtration rate (eGFR), (3) nephrotic proteinuria and (4) hematuria. Results We analysed 72 patients with T2DM that were submitted to KB (Table 1). All except one patient had hypertension and 38 patients were screened for diabetic retinopathy (DR), which was present in 23 patients (60%). The criteria for KB was in most of the patients (59.7%) a low or rapidly declining eGFR, followed by nephrotic proteinuria (19.4%), nephrotic syndrome (16.7%) and hematuria (4.2%). KB showed 50% (n = 36) of patients with NDKD, 12.5% (n = 9) with NDKD and DKD and 37.5% (n = 27) with isolated NDKD. Among these patients, hypertensive nephrosclerosis (19.4%), focal segmental glomerulosclerosis (13.8%), acute interstitial nephritis (13.8%), membranous nephropathy (11.2%) and IgA nephropathy (5.6%), were the most prevalent diagnosis. Patients with DR had a higher prevalence of DKD with a positive predictive value (PPV) of 87%. On the other hand, in the absence of DR, DKD was only absent in 66.7%. Patients submitted to KB for the criteria of low or rapid declining eGFR had significantly more NDKD (p = 0.016). DKD with or without NDKD was found in patients with higher levels of albumin to creatinine ratio (p = 0.001) and HbA1c (p = 0.05). Conclusion Our data showed that NDKD is prevalent in T2DM patients, and given its potentially treatable nature, KB should be considered in T2DM patients, especially in those with low or rapid declining eGFR. DR supports the diagnosis of DKD (PPV of 87%), but alone is insufficient to exclude other causes. Patients with DKD had higher levels of albuminuria and HbA1c. Overall, more than half of the patients had hematuria, without any correlation with any group.

#6612 ACUTE KIDNEY INJURY ASSOCIATED WITH IMMUNE CHECKPOINT INHIBITOR THERAPY: REPORT OF 4 CASES

Abstract Background and Aims Immunotherapy using immune check point inhibitors (ICIs) is the cornerstone of modern cancer therapy. Despite significant clinical benefits, ICIs are associated with remarkable adverse events of autoimmune nature involving various organs. Acute Kidney Injury (AKI) occurs more rarely, mainly with the appearance of acute interstitial nephritis. We present a series of patients with AKI after administration of immunotherapy with ICIs. Method Patient 1 with metastatic small cell lung cancer on immunotherapy with atezolizumab presented with purpura on the trunk and lower extremities, AKI, microscopic glomerular hematuria, and proteinuria. Patient 2 with esophageal malignancy on immunotherapy with pembrolizumab and worsening renal function. Patient 3 with endometrial malignancy on immunotherapy with pembrolizumab developed AKI, nephrotic syndrome and microscopic hematuria. Patient 4 with melanoma on immunotherapy with pembrolizumab presented with microscopic hematuria and rash. Results A kidney biopsy was performed in all 4 patients unreavealling the following; Patient 1: pauci-immune necrotizing glomerulonephritis with fibrinoid necrosis and inflammation in the wall of a vessel. Patient 2: acute interstitial nephritis with intense inflammation. Patient 3: findings consistent with focal segmental glomerulosclerosis (FSGS, NOS), without evidence of immune complex disease. Patient 4: focal segmental glomerulosclerosis, moderate interstitial fibrosis and interstitial nephritis in remission. The patient had already been treated with glucocorticoid. In all 4 patients immunotherapy was temporarily discontinued and they were treated with intravenous pulses of methyl-prednisolone followed by oral glucocorticoids, with significant improvement of kidney function and resolution of all extra renal manifestation i.e skin rash etc. Escalation of immunosuppressive therapy with the addition of another agent was avoided in order not to cause relapse of the malignancy. Conclusion AKI is a rare but potentially serious complication of ICIs. Temporal discontinuation of the implicated agent is of major importance while treatment with glucocorticoids may be critical for kindey function. Yet, constant vigilance and sustained collaboration among medical specialists are becoming essential in the increasing use of immunotherapy.

Renal diseases causing hematuria

Background: Hematuria is a common laboratory finding in clinical practice, occurring mostly in the kidneys. However, it can occur in the rest of the urinary system, including the ureters, bladder, and urethra, as well as in the prostate in men. This paper will discuss cases of hematuria observed in various diseases, especially kidney disease.Current Concepts: Hematuria is diagnosed when three or more red blood cells are found in a high-power field microscopic urinalysis. Identifying urine sediment is critical in differentiating between glomerular and nonglomerular hematuria, classified according to location. If hematuria is accompanied by proteinuria, dysmorphic red blood cells, or cellular casts in urine microscopy, as well as hypertension or renal function decline, glomerular disease may be present; thus, a nephrologist should be consulted. Hematuria is also observed in renal vascular diseases, including renal infarction, renal artery dissection, and nutcracker syndrome. In polycystic kidney disease, hematuria may present in combination with renal stones or malignancy. Diabetic nephropathy can manifest hematuria, which is a negative prognosticator of end-stage kidney disease.Discussion and Conclusion: Hematuria is a laboratory finding for various diseases, and appropriate diagnosis and treatment should be provided according to its clinical features.

Assessing physical inactivity as a risk factor for chronic kidney diseases in Iranian population

ObjectivesPhysical inactivity is a major adjustable lifestyle risk factor in renal patients; nevertheless, research on the association of physical activity (PA) with chronic kidney disease (CKD) is unclear.DesignCross-sectional.SettingWe evaluated the...

Proliferative glomerulonephritis with monoclonal IgG deposits: a unique case with a clinical course of over 46 years

BackgroundProliferative glomerulonephritis with monoclonal IgG deposits (PGNMID) is a rare entity first described in 2004. We present a case of PGNMID with recurrent hematuria and nephrotic range proteinuria with three biopsies over 46 years.Case presentationA 79-year-old Caucasian female presents with a history of two separate episodes of biopsy-proven recurrent GN over a course of 46 years. Both biopsies from 1974, and 1987 were reported as membranoproliferative GN (MPGN). The patient presented in 2016 for the third time with symptoms of fluid overload, slight worsening in renal function, and proteinuria along with glomerular hematuria. A third kidney biopsy was performed, and the final diagnosis was proliferative glomerulonephritis with monoclonal IgG/κ deposits.ConclusionWith three renal biopsies obtained over 46 years, our case opens a unique window into the natural history of PGNMID. The three biopsies demonstrate the immunologic and morphologic evolution of PGNMID in the kidney.

Τhe Impact of Pre-Transplant Kidney Biopsy on the Evaluation of Prospective Living Kidney Donors

Living kidney donation contributes to increasing the donor pool. Since safety and excellent outcomes of living kidney donors (LKD) are essential, renal biopsy must be part of the pre-transplant evaluation in donors with isolated urine abnormalities or other risk factors. We retrospectively collected data on potential living donors evaluated in the pre-transplant outpatient clinic of Laiko General Hospital of Athens between 2007 and 2022, who underwent a pre-transplant biopsy. Biopsy indications included microscopic hematuria, borderline proteinuria and comorbidities suggestive of chronicity. Those with glomerular diseases or chronic lesions were excluded from donation. We identified 59 potential living donors who underwent renal biopsy. Of these, 10 (16.9%) were male. Median age was 58 (IQR 51-63) years, while 23 (39%) were older than 60 years. 49 out of 59 (83%) had glomerular hematuria, 10 (16.7%) had proteinuria (150-300 mg/d). Out of the 59 donors, 21 (35.6%) were hypertensive, three (5.1%) had impaired glucose tolerance and seven (11.9%) had a BMI > 30 kg/m2. A total of 32 (54.2%) potential donors were accepted for donation. Eight (13.6%) had IgA nephropathy, 10 (16.9%) TBMD and nine (15.3%) had increased chronicity including secondary FSGS. When compared with a control group of donors who did not need a pre-transplant biopsy, those 32 who donated were more frequently hypertensive (p = 0.003), but had similar eGFR [61.3 (±10.4) vs. 61.9 (±13.8), p = 0.866] after a follow-up of 79 (36-114) months. Renal biopsy is a useful tool in the evaluation of prospective LKD. Thorough assessment of donors with isolated urine abnormalities and marginal donors is critical to ensure good post-donation outcomes.

The Impact of BMI Changes on the Incidence of Glomerular Hematuria in Korean Adults: A Retrospective Study Based on the NHIS-HEALS Cohort

Obesity and recurrent hematuria are known risk factors for chronic kidney disease. However, there has been controversy on the association between obesity and glomerular hematuria. This study aimed to investigate the association between body mass index (BMI) and weight change and recurrent and persistent hematuria in glomerular disease using a large-scale, population-based Korean cohort. Data were collected from the National Health Insurance Service-National Health Screening Cohort. Cox proportional hazards regression analysis was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for recurrent and persistent hematuria in glomerular disease according to the BMI group. Compared with the BMI 23-25 kg/m2 group, the HR (95% CI) for incident recurrent and persistent hematuria in glomerular disease was 0.921 (0.831-1.021) in the BMI <23 kg/m2 group, 0.915 (0.823-1.018) in the BMI 25-30 kg/m2 group, and 1.151 (0.907-1.462) in the BMI ≥30 kg/m2 group. Compared with the stable weight group, the HRs (95% CIs) for incident recurrent and persistent hematuria in glomerular disease were 1.364 (1.029-1.808) and 0.985 (0.733-1.325) in the significant weight loss and gain groups, respectively. Despite adjusting for confounders, this result remained significant. Baseline BMI was not associated with the risk of incident recurrent and persistent hematuria in glomerular disease. Weight loss greater than 10% was associated with the incidence of recurrent and persistent hematuria in glomerular disease. Therefore, maintaining an individual's weight could help prevent recurrent and persistent hematuria in glomerular disease in middle-aged and older Korean adults.

Rapidly Progressive Pauci-Immune Glomerulonephritis with Aberrant Fibrinoid Necrosis Associated with Atezolizumab, an Immune Check Point Inhibitor: A Case Report and Review of Literature

Stimulation of the antitumor activity of the immune system using immune checkpoint inhibitors (ICIs) has proven efficacy in the treatment of multiple types of cancer, inducing the speedily expanding approval of therapeutic indications for ICIs. The literature regarding the immune-related toxicities and nephrotoxicity of ICIs is limited. Herein, we present a patient with lung cancer treated with atezolizumab, an IgG1 monoclonal antibody aimed at the programmed death ligand 1 (PD-L1), who presented with vasculitic skin rash and rapidly deteriorating renal function, new onset of significant glomerular hematuria and proteinuria. The renal biopsy revealed acute necrotizing pauci-immune vasculitis, with fibrinoid necrosis. The patient received a course of high-dose glucocorticoids with recovery of renal function and skin lesions. Further immunosuppressive therapy was withheld, due to active malignancy in the lung, while oncology consultation recommended the continuation of treatment with atezolizumab, as the patient had shown substantial response.

Kidney outcome after mild to moderate COVID-19.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has a remarkable kidney tropism. While kidney effects are common in severe coronavirus disease 2019 (COVID-19), data on non-severe courses are limited. Here we provide a multilevel analysis of kidney outcomes after non-severe COVID-19 to test for eventual kidney sequela. This cross-sectional study investigates individuals after COVID-19 and matched controls recruited from the Hamburg City Health Study (HCHS) and its COVID-19 program. The HCHS is a prospective population-based cohort study within the city of Hamburg, Germany. During the COVID-19 pandemic the study additionally recruited subjects after polymerase chain reaction-confirmed SARS-CoV-2 infections. Matching was performed by age, sex and education. Main outcomes were estimated glomerular filtration rate (eGFR), albuminuria, Dickkopf3, haematuria and pyuria. A total of 443 subjects in a median of 9months after non-severe COVID-19 were compared with 1328 non-COVID-19 subjects. The mean eGFR was mildly lower in post-COVID-19 than non-COVID-19 subjects, even after adjusting for known risk factors {β=-1.84 [95% confidence interval (CI) -3.16 to -0.52]}. However, chronic kidney disease [odds ratio (OR) 0.90 (95% CI 0.48-1.66)] or severely increased albuminuria [OR 0.76 (95% CI 0.49-1.09)] equally occurred in post-COVID-19 and non-COVID-19 subjects. Haematuria, pyuria and proteinuria were also similar between the two cohorts, suggesting no ongoing kidney injury after non-severe COVID-19. Further, Dickkopf3 was not increased in the post-COVID-19 cohort, indicating no systematic risk for ongoing GFR decline [β=-72.19 (95% CI -130.0 to -14.4)]. While mean eGFR was slightly lower in subjects after non-severe COVID-19, there was no evidence for ongoing or progressive kidney sequela.

Challenges of defining renal response in ANCA-associated vasculitis: call to action?

Avoiding end-stage kidney disease in patients with anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) has a high therapeutic priority. Although renal response is a crucial measure to capture clinically relevant changes, clinal trials have used various definitions and no well-studied key surrogate markers to predict renal outcome in AAV exist. Differences in clinical features and histopathologic and therapeutic approaches will influence the course of kidney function. Its assessment through traditional surrogates (i.e. serum creatinine, glomerular filtration rate, proteinuria, hematuria and disease activity scores) has limitations. Refinement of these markers and the incorporation of novel approaches such as the assessment of histopathological changes using cutting-edge molecular and machine learning mechanisms or new biomarkers could significantly improve prognostication. The timing is favourable since large datasets of trials conducted in AAV are available and provide a valuable resource to establish renal surrogate markers and, likely, aim to investigate optimized and tailored treatment approaches according to a renal response score. In this review we discuss important points missed in the assessment of kidney function in patients with AAV and point towards the importance of defining renal response and clinically important short- and long-term predictors of renal outcome.