Journal of nephropathology
Volume:10 Issue: 2, Apr 2021

Pigment cast nephropathy is one of the most severe complications of rhabdomyolysis. It is an important cause of renal failure requiring renal replacement therapy. We report the case of a 23-year-old man who presented with short febrile illness with hyperpyrexia and altered sensorium. Non-contrast CT-brain and CSF analysis were normal. He later developed petechial rashes with thrombocytopenia followed by frank hematuria and worsening renal functions. A kidney biopsy was performed, which revealed findings of myoglobin cast nephropathy

IgA nephropathy (IgAN) is the most common primary glomerulonephritis (GN) in western countries and Henoch-Schönlein purpura nephritis (HSPN) is the most common form of vasculitis in childhood. Renal biopsy findings in both nephropathies are often similar and are characterized by mesangioproliferative GN with mesangial or mesangiocapillary IgA and C3c deposits.

The aim of this study was to investigate the significance of glomerular C4d-deposition as a discriminating factor between pediatric HSPN and IgAN. Patients and

We retrospectively analyzed patient records and renal biopsies from 53 pediatric patients from one single center with a median age of 10.5 years (range 2.3-18 years). Twenty-two patients suffered from IgAN and 31 from HSPN. Work-up of all renal biopsies was performed using standard protocols including immunohistochemistry for C4d.

Pediatric IgAN patients presented significantly more often with gross hematuria, higher serum creatinine, lower glomerular filtration rate, lower serum C3 and proteinuria and on histology less endocapillary hypercellularity compared to HSPN patients. However, the rate of glomerular C4d-positivity was not different between IgAN (36%) and HSPN (42%). Comparing all cases with positive versus negative glomerular C4d-staining, pediatric patients with glomerular C4d-positivity showed significantly lesser gross hematuria and received significantly more often cyclophosphamide. This was in line with a tendency towards more proteinuria, hypertension and renal insufficiency at last follow-up in C4d-positive compared to C4d-negative patients.

In conclusion, in our monocentric study glomerular C4d does not differ between pediatric HSPN and IgAN, but was associated with a tendency to a more severe course of the disease that needs to be confirmed in larger multicentric studies.

Diabetes is an illness of epidemic magnitude, and the figures are rising each year. Diabetic nephropathy (DN) is a dreaded long-term complication of diabetes and the most common reason for end-stage renal disease (ESRD). Microalbuminuria is considered as a non-invasive indicator of early onset of DN. Renal biopsy is vital to know the extent of renal damage. Vascular endothelial growth factor (VEGF) plays a key role in angiogenesis and has been implicated in the pathogenesis and development of the disease.

To assess the expression of VEGF in different classes of DN and to evaluate its association with the known clinical and histopathological prognostic factors. Patients and

Fifty-five patients of DN undergoing a renal biopsy were studied and classified according to the “pathologic classification of DN” by Tervaert et al. Glomerular and tubular staining of VEGF was recorded. P values of less than 0.05 were considered statistically significant.

Of 55 patients, eight patients belonged to class II, 24 to class III, and 23 to class IV. VEGF was positive in six (75%) of class II, 17 (70.83%) of class III and eight (34.7%) of class IV biopsies. A statistically significant correlation between classes of DN with estimated glomerular filtration rate (eGFR), serum creatinine, serum urea, diabetic retinopathy, hematuria, VEGF positivity and staining intensity was observed.

A precise assessment of renal damage in DN can be conducted by studying renal biopsies. VEGF expression is increased in the early stage of diabetes however; further studies could open up new avenues for early diagnosis and management.

The evolution of structural changes of diabetic nephropathy in human kidneys is not well documented. Instead, rodent models are used to study diabetic nephropathy in greater detail. However, all rodent models to date are subject to important limitations, and not representative for the more complex human setting where type 2 diabetes mellitus is often accompanied by the metabolic syndrome, induced by a high-fructose western diet.

To evaluate whether a novel mouse model of metabolic syndrome could be used as valid model for preclinical studies on diabetic nephropathy.

We established a model of type 2 diabetes mellitus induced by a highsucrose/high-fat (HSHF) diet in female LDL-receptor knockout C57BL/6J mice and used manual morphometry to examine the renal histological changes in this model.

The HSHF diet induced a metabolic syndrome with weight gain, hyperinsulinemia, insulin resistance, type 2 diabetes mellitus, and hyperlipidemia. After 16 weeks on the HSHF diet, morphometric examination of kidney biopsies demonstrated increased mesangial matrix expansion, no glomerulosclerosis, and only discrete morphological changes in glomeruli. Mesangial matrix expansion was highly correlated with biological features of the metabolic syndrome.

We describe a novel, accessible mouse model with features of the metabolic syndrome and development of mesangial matrix expansion. This model is comparable to the human setting and could serve as a relevant experimental model for nephropathy associated with type 2 diabetes mellitus. By assessing both morphological and morphometric features we demonstrated the increased sensitivity and more detailed evaluation of manual morphometry over visual estimation by light microscopy

Introduction: 

The high transmissibility and lethality of the novel coronavirus SARS-CoV-2 (COVID-19) have been catastrophic. Acute kidney injury (AKI) is one of the frequent complications in patients with respiratory insufficiency caused by the virus. The pathogenic mechanism is based on the binding of its S-proteins to the angiotensin-converting enzyme (ACE) receptors, which will trigger a cellular damage. A podocyte and tubular compromise are found in the kidneys which can lead to tubular necrosis and the consequent AKI. Objectives: The objective of this report is to identify the main risk factor to develop AKI in patients infected with SARS-CoV-2 with critical acute respiratory distress.

Patients and Methods:

 We performed this report study, collecting data from 48 ICU patients. Data from 13 of them who developed AKI and needed renal replacement therapy (RRT)were analyzed. Clinical characteristics and laboratory findings were reported using STATA 10.0.

Results: 

AKI was present in 27.08% of patients, mostly male (92.3%) with a mean age of 63.8 years old. Hypertension, diabetes and obesity were the main comorbidities in those patients. Additionally, the meantime between admission and AKI diagnosis was 2.69 days. All patients showed fibrinogen, D-dimer, ALT and values above normal range. Mortality was seen in 61.5% of patients.

Conclusion: 

This report tries to show AKI as an important clinical manifestation in critically ill patients infected with SARS-CoV-2, with high mortality. Further studies are needed to demonstrate if there are independent risk factors.

Lupus nephritis (LN) is a renal manifestation of systemic lupus erythematosus (SLE), an autoimmune disease more common in females. Clinicopathological manifestations and outcomes of LN in males are uncertain.

To assess and compare clinicopathological manifestations and outcomes of males and females with LN. Patients and

Patients with LN were identified from database (male 94, female 344). Clinical manifestations, laboratory data, renal histopathology and outcome were retrieved and compared.

Compared to females, males were more likely to present with rapidly progressive glomerulonephritis (RPGN) (21.3% versus 11.6%, P = 0.026) and low-serum complement (76.6% versus 63.7%, P = 0.019). While asymptomatic hematuria and/or proteinuria was the second most common clinical manifestation in females (40%), no males presented with this manifestation. Although LN class IV was most common in both groups, males were more likely to have LN class IV with most severe form of renal manifestation than females (50% versus 38.7%, P = 0.048). Males showed tendency for poorer renal survival, but without statistical significance.

Males with LN had more severe clinicopathological manifestations than females. Clinicians should be aware of SLE with LN in males in order to make timely diagnosis and treatment.

Kidney is one of the most common organs affected by coronavirus disease 2019 (COVID-19) after the respiratory and immune systems. Among the renal parenchymal components, the tubulointerstitial compartment is presumed to be the prime target of injury in COVID-19. The main mechanism of renal tubular damage by COVID-19 is considered to be indirect, i.e., cytokine-mediated injury. A proportion of infected individuals mount a strong inflammatory response to the virus by an exaggerated immune response of the body, namely cytokine storm. Sudden and massive release of cytokines may lead to serious systemic hyper-inflammation and renal tubular injury and inflammation resulting in acute renal failure. In addition, a number of cases of glomerulopathies, particularly collapsing glomerulopathy (CG) have been reported, predominantly in people of African ancestry, as a rare form of kidney involvement by SARS-CoV-2 that may originate from the background genetic susceptibility in this population complicated by the second hit of SARS-CoV-2 infection, either directly or indirectly. It is noteworthy that renal injury in COVID-19 could be severe in individuals of African origin due to the aforementioned genetic susceptibility, especially the presence of high-risk apolipoprotein L1 (APOL1) genotypes. Although the exact mechanism of kidney injury by SARS-CoV-2 is as yet unknown, multiple mechanisms are likely involved in renal damage caused by this virus. This review was aimed to summarize the salient points of pathogenesis of kidney injury, particularly glomerular injury in COVID-19 disease in the light of published data. A clear understanding of these is imperative for the proper management of these cases. For this review, a search was made of Google Scholar, Web of Science, Scopus, EBSCO and PubMed for finding English language articles related to COVID-19, kidney injury and glomerulopathy. From the information given in finally selected papers, the key aspects regarding glomerular involvement in COVID-19 were drawn out and are presented in this descriptive review.

Remdesivir initially was intravenously administrated to treat the Ebola disease however right now it has been administered to treat COVID-19 in some countries. However it is necessary to find the exact effect of remdesivir in patients with COVID-19. Remdesivir solution is administered with a cyclodextrin carrier that filters solely by the glomeruli; thereby patients with abnormal renal function cannot eliminate it quickly; therefore, remdesivir can lead to renal failure or liver dysfunction during therapeutic process of COVID-19. Assessment of renal function in patients with COVID-19 who have acute kidney injury (AKI) or end-stage renal disease is fundamental.

Lung cancer is the leading cause of cancer deaths worldwide, accounting for an estimated 1.8 million deaths. Lung cancer is also the most common primary cancer leading to soft tissue (ST) metastasis. Renal disease may occur as a direct or indirect consequence of the cancer itself (e.g., postrenal obstruction, compression, or infiltration), its treatment (e.g., radiotherapy or chemotherapy), or its related complications (e.g., opportunistic infection). Existing evidence shows that the most frequent primary solid tumor responsible for renal metastasis is pulmonary carcinoma, followed by gastric, breast, soft tissue, and thyroid carcinomas. Chronic kidney disease is a potential risk factor in the survival of patients with lung cancer. In this review, we will discuss causes of kidney injury in relation to lung cancer, potential mechanisms of kidney injury, and treatment options.

AA amyloidosis is a complication related to several chronic inflammatory conditions like cancer, autoimmune diseases and infections, among others. The disease implicates amyloid fibrils deposit in tissues leading to organ failure. Renal involvement has been closely associated with amyloidosis and sometimes with tuberculosis too. Therefore, it is important to achieve a renal biopsy that allows elucidating the etiology of the clinical picture in order to provide the correct treatment to the patients. In this paper, we present a case of renal amyloidosis secondary to pulmonary tuberculosis which debuted as nephrotic syndrome.

Cryoglobulinemia is a condition where complexes of one or more different classes of immunoglobulins precipitate at low temperatures and become soluble again at higher temperatures. Cryoglobulins are typically categorized as types I to III, based on their immunoglobulin composition. Mixed cryoglobulinemia (type II and III) is most often associated with constitutional symptoms, such as fatigue, myalgia, arthralgia, sensory or motor changes (peripheral neuropathy) and palpable purpura (cutaneous vasculitis). Twenty to thirty percent of the affected patients suffer from membranoproliferative glomerulonephritis. Case Presentaion: We discuss a case of a 45-year-old woman with a history of Sjögren’s syndrome and mixed cryoglobulinemia who presented with acute renal failure, nephritic syndrome, vasculitislike rash on the legs and non-healing skin ulcer. Further investigations confirmed type II mixed cryoglobulinemia associated with cutaneous leukocytoclastic vasculitis and membranoproliferative glomerulonephritis leading to end-stage renal disease (ESRD).

Mixed cryoglobulinemia secondary to primary Sjögren’s syndrome (pSS) is rare and reported in 22.5% of cases of non-infectious cryoglobulinemic glomerulonephritis. Long-term renal prognosis is good with only 9% of these patients evolving to ESRD. Nevertheless, the long-term overall survival is poor with severe infections as the leading cause of death.

Cholesterol crystals and granulomas in tubular lumen and interstitium of the kidney are infrequent findings during nephrotic syndrome (NS) and are poorly described. We attempt to discuss cholesterol crystals in NS as a form of crystallopathy.

Three cases of 207 (1.5%) performed kidney biopsies, between 2001 and 2019, in patients with NS, showed cholesterol crystals deposition in tubules, interstitium and even cholesterol granulomas with some degree of interstitial mononuclear inflammation with giant cells, interstitial fibrosis and variable tubular atrophy. Oil Red O staining revealed lipid laden macrophages in interstitium and lipid droplets in tubular epithelium. Two patients had membranous glomerulonephritis (MGN) and one membranoproliferative glomerulonephritis (MPGN). The proteinuria ranged from 6.08 to 12.57 g/24 hours, lasting from 1 to 22 months. All had hypertension, high values of serum cholesterol and triglycerides.

Clinically significant deposition of cholesterol crystals in kidney is mainly in atheroembolic renal disease, however deposition of cholesterol crystals during NS is rare and it is not considered a form of crystallopathy. Cholesterol crystals do not seem to be correlated with degree of proteinuria, persistence of NS or type of glomerulonephritis, but it is correlated with amount of serum cholesterol which is strongly associated with the severity of NS. Therefore we propose it as tubular crystallopathy, in the setting of NS associated hypercholesterolemia which may cause chronic kidney disease (CKD).