Glomerulosclerosis
| Glomerulosclerosis | |
|---|---|
| Other names | Glomerular sclerosis |
| Specialty | Nephrology |
Glomerulosclerosis is the hardening of the glomeruli in the kidney, which hinders the kidneys' ability to properly filter blood and can result in kidney disease. It is a general term to describe scarring of the kidneys' glomeruli, the tiny blood vessels that serve as the functional units in the kidney for filtration of the blood.
Both children and adults can develop glomerulosclerosis which can result from different types of kidney conditions. Nodular glomerulosclerosis is one frequently encountered type of glomerulosclerosis and is caused by diabetes. Focal segmental glomerulosclerosis (FSGS) is another type of glomerulosclerosis and can result from malignancies, drugs, infections, or genetic inheritance, though it may also occur without an identifiable cause.
Proteinuria (large amounts of protein in the urine) is the major sign of glomerulosclerosis. Scarring disturbs the filtering process of the kidneys and allows protein to leak from the blood into the urine. Symptoms of glomerulosclerosis may include swelling, fatigue, nausea and vomiting, itchy skin, poor appetite, or shortness breath, among others.
A kidney biopsy (the sampling of a tiny part of the kidney with a needle) may be necessary to determine whether a patient has glomerulosclerosis or another kidney problem. Kidney biopsy of a patient with glomerulosclerosis may show glomerular scarring and podocyte damage, as well as more specific findings associated with each type of glomerulosclerosis.
Treatment of glomerulosclerosis depends on the type, but may include medications for blood pressure control, steroids, or kidney transplant, depending on the severity.
Types
More specifically, glomerulosclerosis can refer to:
Signs and symptoms
The hallmark sign of glomerulosclerosis is proteinuria, which refers to the leaking of protein into urine as it is filtered through the kidneys.[1][2] Though patients can be otherwise asymptomatic in the presence of proteinuria, progression of kidney disease can result in further complications, such as swelling, uremia, fatigue, headache, nausea and vomiting, poor appetite, shortness of breath, irregular heartbeat, or itchy skin.[3][4] Severe and untreated disease is associated with poor cardiovascular outcomes and progression to end-stage renal disease (ESRD).[4][5]
Diagnosis
Evaluation for glomerulosclerosis usually begins with a urine study to determine the presence of proteinuria. In the case of FSGS, this may be initiated by the abrupt onset of nephrotic syndrome (leaking of greater than 3.5g/day) or evidence of worsening kidney function on routine laboratory evaluation.[6] In the case of nodular glomerulosclerosis, screening for microalbuminuria is performed annually and is initiated either 5 years after diagnosis with type 1 diabetes or upon diagnosis with type 2 diabetes.[7] In both cases, the discovery of otherwise unexplained proteinuria usually warrants further workup by a kidney biopsy for histological evaluation, including histochemistry, immunofluorescence, and electron microscopy.[8]
Treatment
Treatment for glomerulosclerosis depends on what caused the scarring of the glomeruli. This is determined by a renal biopsy. Immunosuppressive drugs stop proteinuria in some patients, but once the treatments have ended, proteinuria will continue. The drugs may sometimes damage the patient's kidneys even more.
Controlling the patient's blood pressure may control the progression of kidney failure. ACE inhibitors, a type of blood pressure medicine, preserve kidney function in patients with diabetes. ACE inhibitors may also slow down kidney failure in patients without diabetes. Low-protein diets may also lessen the work done by the kidneys to process waste. Some patients will need to control their cholesterol through diet or both diet and medicine.
See also
References
- ^ Sun, Ke; Xie, Qionghong; Hao, Chuan-Ming (2021). "Mechanisms of Scarring in Focal Segmental Glomerulosclerosis". Kidney Diseases. 7 (5): 350–358. doi:10.1159/000517108. ISSN 2296-9381. PMC 8443927. PMID 34604342.
- ^ Doshi, Simit M.; Friedman, Allon N. (August 2017). "Diagnosis and Management of Type 2 Diabetic Kidney Disease". Clinical Journal of the American Society of Nephrology. 12 (8): 1366–1373. doi:10.2215/CJN.11111016. ISSN 1555-9041. PMC 5544517. PMID 28280116.
- ^ "Diabetes and kidney disease: MedlinePlus Medical Encyclopedia". medlineplus.gov. Retrieved 2026-03-17.
- ^ a b Altintas, Mehmet M.; Agarwal, Shivangi; Sudhini, Yashwanth; Zhu, Ke; Wei, Changli; Reiser, Jochen (2025-01-24). "Pathogenesis of Focal Segmental Glomerulosclerosis and Related Disorders". Annual Review of Pathology: Mechanisms of Disease. 20 (1): 329–353. doi:10.1146/annurev-pathol-051220-092001. ISSN 1553-4006. PMC 11875227. PMID 39854184.
- ^ Doshi, Simit M.; Friedman, Allon N. (2017-08-07). "Diagnosis and Management of Type 2 Diabetic Kidney Disease". Clinical Journal of the American Society of Nephrology. 12 (8): 1366–1373. doi:10.2215/CJN.11111016. ISSN 1555-905X. PMC 5544517. PMID 28280116.
- ^ Zhu, Yan; Xu, Gaosi (2025). "Advances in Focal Segmental Glomerulosclerosis Treatment From the Perspective of the Newest Mechanisms of Podocyte Injury". Drug Design, Development and Therapy. 19: 857–875. doi:10.2147/DDDT.S498457. ISSN 1177-8881. PMC 11812565. PMID 39935575.
- ^ Samsu, Nur (January 2021). Bellini, Maria Irene (ed.). "Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment". BioMed Research International. 2021 (1) 1497449. doi:10.1155/2021/1497449. ISSN 2314-6133. PMC 8285185. PMID 34307650.
- ^ Mateus, Catarina; Cacheira, Eunice; Laranjinha, Ivo; Dickson, Jorge; Gaspar, Augusta (2022). "Non-diabetic metabolic nodular glomerulosclerosis". Clinical Nephrology. Case Studies. 10: 82–86. doi:10.5414/CNCS110943. ISSN 2196-5293. PMC 9746242. PMID 36524200.