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Glomerulosclerosis
Published in Charles Theisler, Adjuvant Medical Care, 2023
Glomeruli are the functional units of the kidneys that enable nephrons to filter waste products such as urea out of the blood. Glomerulosclerosis is scarring or hardening of the glomeruli. This damage can result in proteinuria (loss of large amounts of protein [i.e., albumen] from the blood into the urine), microscopic hematuria (blood and casts in the urine), hypertension, and the nephrotic syndrome (proteinuria plus low albumen and high fat in the blood along with edema in the legs feet or ankles). Glomerulosclerosis may develop in children or adults. African Americans are at higher risk.
Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Glomerular disease can be classified according to the clinical syndrome produced, the histopathological appearance or the underlying disease. Glomerular disease is primary if there is no other system affected and secondary if there is another system affected (the renal disease is considered secondary to the systemic condition). The glomerulus consists of the glomerular basement membrane, the glomerular cells, the intraglomerular blood vessels and the mesangium (the supporting connective tissue). Glomerular disease can affect one or more of these components.
Potential of Fenugreek in Management of Kidney and Lung Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Amit D. Kandhare, Anwesha A. Mukherjee-Kandhare, Subhash L. Bodhankar
Glomerulonephritis or nephritis is a severe and life-threatening illness that occurs due to inflammation of the glomeruli. Although prevalence is low, nephritis can be rapidly progressive and the patient may need immediate treatment. Additionally, damage to the glomerulus results in arterial hypertension and renal failure. Glomerulonephritis includes many diseases, namely anti- GBM antibody disease, IgA nephropathy, lupus nephritis, and ANCA-associated vasculitis (McAdoo and Pusey 2017). The pathophysiology remains unknown for glomerulonephritis; however, bacterial and viral infections have been encountered frequently during a clinical investigation (Couser and Johnson 2014). The recommended treatment regimen for glomerulonephritis includes daily administration of oral steroids such as cyclophosphamide and plasma exchange to decrease the serum levels of anti-GBM antibodies. Although these therapies are more efficient in removing antibodies from serum, their cost and availability have acted as limitations in widespread clinical practice.
Antiandrogen enzalutamide induced genetic, cellular, and hepatic damages: amelioration by triterpene Lupeol
Published in Drug and Chemical Toxicology, 2023
Mohammad A. Khan, Deepti Singh, Homa Fatma, Kafil Akhtar, Farruk Arjmand, Santosh Maurya, Hifzur R. Siddique
Next, kidney sections of the control group showed normal glomeruli (G) with mesangial capillaries and normal-sized tubules (T). Lupeol treated group also showed normal kidney glomeruli (G) with mesangial capillaries and cuboidal epithelium lined tubules (T) with mild lymphocytic infiltrate in the interstitium (+) (L). However, Enzalutamide treated group revealed some histological distortions, such as kidney glomeruli with a proliferation of mesangial capillaries (2+) (G) with focally atrophied tubules (T) and a moderate degree of interstitial hemorrhage (2+) (H). Interestingly, the sections of the combination-treated group showed a different pattern in the upper and lower half. The upper-half revealed congested blood capillaries (+) with dilated blood vessels (V), atrophied, and focally necrosed tubules (T). However, in the lower-half, focally normal tubules were observed (Figure 5(A–H)). A summary of the results of histopathological examination of liver and kidney in the animals exposed to the test chemical for 48 hrs is presented in Table 2.
Renal and overall outcomes of double-positive (ANCA and anti-GBM antibodies) patients compared to ANCA-associated vasculitis patients with severe renal involvement: A multicenter retrospective study with systematic renal pathology analysis
Published in Scandinavian Journal of Rheumatology, 2022
M Clerte, R Philip, C Levi, E Cornec-Le Gall, V Audard, A Huart, X Puéchal, M Touzot, N Rabot, É Thervet, A Aouba, A Karras
Renal biopsy was performed for all patients, revealing linear deposition of IgG and complement along the GBM. Detailed biopsy analysis was available for 30 of them (90%). Light microscopy revealed an average of 18 ± 8 glomeruli per biopsy. Only seven renal biopsies (23%) showed diffuse and active crescentic glomerulonephritis in all glomeruli present on the biopsy sample, corresponding to a severe, acute, first, ongoing flare of the disease. Twenty-three renal biopsies (77%) showed sclerotic glomeruli, with a median percentage of 20% (4–86%), corresponding to previous and scarred kidney injury. Finally, only 12 renal biopsies (40%) found some normal glomeruli with a median percentage of normal glomeruli of 10% (6–29%). Nine patients had interstitial fibrosis, with a median of 35% (0–50%) fibrotic involvement.
Concomitant rapidly progressive glomerulonephritis and acute rheumatic fever after streptococcus infection: a case report
Published in Paediatrics and International Child Health, 2022
Suwanna Pornrattanarungsi, Sudarat Eursiriwan, Yupaporn Amornchaicharoensuk, Chutima Chavanisakun, Ornatcha Sirimongkolchaiyakul
Acute post-streptococcal glomerulonephritis (APSGN) and acute rheumatic fever (ARF) are common, non-suppurative disorders which occur after group A streptococcal (GAS) infection, especially acute pharyngitis or skin infection [1,2]. Typical clinical manifestations in acute glomerulonephritis are hypertension, oedema and glomerular haematuria. Acute rheumatic fever may be associated with cardiac lesions together with systemic signs and symptoms such as polyarthritis, chorea, erythema marginatum, fever and increased inflammatory markers. The diagnosis of APSGN or ARF requires laboratory evidence of preceding streptococcal infection. However, the main mechanism underlying both diseases varies. Immune complex formation is the crucial pathogenesis of APSGN whilst ARF can arise as a result of molecular mimicry [3]. Rarely, however, both occur simultaneously.