Nephritic syndrome#Causes

File:MicroHematuria.JPG (one of the symptoms of Nephritic syndrome]]

Historically, nephritic syndrome has been characterized by blood in the urine (hematuria), high blood pressure (hypertension), decreased urine output <400 ml/day (oliguria), red blood cell casts, pyuria, and mild to moderate proteinuria.{{Cite book|title=Medical physiology : the big picture|last=Kibble|first=Jonathan David|date=2009|publisher=McGraw-Hill|others=Halsey, Colby Ray.|isbn=978-0-07-164302-3|location=New York|pages=221|oclc=469141953}} If the condition is allowed to progress without treatment, it can eventually lead to azotemia and uremic symptoms. This constellation of symptoms contrasts with the classical presentation of nephrotic syndrome (excessive proteinuria >3.5 g/day, low plasma albumin levels (hypoalbuminemia) <3 g/L, generalized edema, and hyperlipidemia).{{Cite book|title = Comprehensive Clinical Nephrology|doi=10.1016/B978-0-323-05876-6.00015-0|publisher = Mosby|date = 2010|page=198|isbn = 9780323058766|first1 = Jürgen|last1 = Floege|first2 = Richard J.|last2 = Johnson|first3 = John|last3 = Feehally|edition = Fourth}}

Signs and symptoms that are consistent with nephritic syndrome include:

• Hematuria (red blood cells in the urine){{Cite book|title = Renal and Electrolyte Disorders|url = https://books.google.com/books?id=3IIqPtg-upwC&q=nephritic+syndrome+hematuria+symptom&pg=PA560|publisher = Lippincott Williams & Wilkins|date = 2010-01-01|page=560|isbn = 9781608310722|first = Robert W.|last = Schrier}}
• Proteinuria (protein in the urine) ranging from sub-nephrotic (<3.5 g/day) to >10 g/day, although it is rarely above nephrotic range proteinuria levels.{{Cite book|url=https://books.google.com/books?id=BRF03rFUZ2YC&pg=PA202|title=Comprehensive Clinical Nephrology E-Book|last1=Floege|first1=Jurgen|last2=Johnson|first2=Richard J.|last3=Feehally|first3=John|date=2010-11-08|publisher=Elsevier Health Sciences|isbn=978-0-323-08133-7|pages=202–203|language=en}}
• Hypertension{{Cite book|title = Atlas of Anatomic Pathology with Imaging: A Correlative Diagnostic Companion|url = https://books.google.com/books?id=6eNHAAAAQBAJ|publisher = Springer Science & Business Media|date = 2013-03-12|page=287|isbn = 9781447128465|first1 = Gerhard R. F.|last1 = Krueger|first2 = L. Maximilian|last2 = Buja}} resting blood pressure is persistently at or above 130/80 or 140/90 mmHg.{{Cite journal|last1=Whelton|first1=Paul K.|last2=Carey|first2=Robert M.|last3=Aronow|first3=Wilbert S.|last4=Casey|first4=Donald E.|last5=Collins|first5=Karen J.|last6=Dennison Himmelfarb|first6=Cheryl|last7=DePalma|first7=Sondra M.|last8=Gidding|first8=Samuel|last9=Jamerson|first9=Kenneth A.|last10=Jones|first10=Daniel W.|last11=MacLaughlin|first11=Eric J.|date=June 2018|title=2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines|journal=Hypertension |volume=71|issue=6|pages=e13–e115|doi=10.1161/HYP.0000000000000065|issn=1524-4563|pmid=29133356|doi-access=free}}
• Blurred vision{{Cite web|title = Acute nephritic syndrome: MedlinePlus Medical Encyclopedia|url = https://www.nlm.nih.gov/medlineplus/ency/article/000495.htm|website = www.nlm.nih.gov|access-date = 2015-10-27}}
• Azotemia (increased plasma Urea and Creatinine){{Cite book|title = Quick Look Nursing: Pathophysiology|url = https://books.google.com/books?id=V3Mf5WhrymYC|publisher = Jones & Bartlett Learning|date = 2008-07-08|page=484|isbn = 9780763749323|first1 = Bernadette|last1 = Madara|first2 = Vanessa|last2 = Pomarico-Denino}}
• Oliguria (low urine output <400 ml/day)
• Red blood cell casts (seen with urinalysis and microscopy){{Cite web|url=http://texascollaborative.org/spencer_urinalysis/ds_sub3.htm|title=Subtopic 3: Microscopic Examination of Urine Sediment|date=November 19, 2004|website=Texas Collaborative|url-status=live|archive-url=https://web.archive.org/web/20041119061730/http://texascollaborative.org/spencer_urinalysis/ds_sub3.htm|archive-date=2004-11-19|access-date=January 22, 2020}}
• Pyuria (white blood cells or pus in the urine)

File:Purpura.jpg

Nephritic syndrome is caused by extensive inflammatory damage to the glomerulus capillaries, which is associated with a variety of medical conditions that we will discuss. Furthermore, the cause of this inflammation can be infectious, autoimmune, or thrombotic.{{Cite book|title = Manual of Nephrology|url = https://books.google.com/books?id=9T21uBxZjj4C|publisher = Lippincott Williams & Wilkins|date = 2008-10-01|pages=144–145|isbn = 9780781796194|language = en|first = Robert W.|last = Schrier}} The causative conditions can be divided conveniently between age groups as follows, though it is important to note that many of the conditions listed in children/adolescents can also occur in adults with lower frequency, and vice versa:

• IgA nephropathy (Note: Contrast time of onset with Post-streptococcal Glomerulonephritis) - Most commonly diagnosed in children who recently had an upper respiratory tract infection (URTI). Symptoms typically present within 1–2 days of a non-specific URI with severe flank/abdominal pain, gross hematuria (characterized by dark brown or red colored urine), and edema of the hands, feet, and/or face.{{Cite journal|last1=Davin|first1=J. C.|last2=Ten Berge|first2=I. J.|last3=Weening|first3=J. J.|date=March 2001|title=What is the difference between IgA nephropathy and Henoch–Schönlein purpura nephritis?|journal=Kidney International|volume=59|issue=3|pages=823–834|doi=10.1046/j.1523-1755.2001.059003823.x|issn=0085-2538|pmid=11231337|doi-access=free}}
• Post-streptococcal glomerulonephritis (PSGN) - Similar to IgA nephropathy, post-streptococcal glomerulonephritis (PSGN) most often occurs in children who have recently had an upper respiratory infection (URI). In contrast with IgA nephropathy, however, PSGN typically presents 2–3 weeks after recovering from an URI that was caused specifically by a Streptococcus bacteria.{{Cite journal|date=2018-12-05|title=Acute Poststreptococcal Glomerulonephritis: Background, Pathophysiology, Epidemiology|url=http://emedicine.medscape.com/article/980685-overview}} The symptoms at onset are very similar to IgA nephropathy and include abdominal pain, hematuria, edema, and oliguria.{{Cite book|title=Comprehensive pediatric nephrology|url=https://archive.org/details/comprehensiveped00mbde|url-access=limited|date=2008|publisher=Mosby/Elsevier|others=Geary, Denis F., Schaefer, Franz.|isbn=978-0-323-07096-6|location=Philadelphia, PA|pages=[https://archive.org/details/comprehensiveped00mbde/page/n307 309]–317|oclc=324995599}}
• Henoch–Schönlein purpura (HSP) - Often considered a systemic form of IgA nephropathy, Henoch–Schönlein purpura (HSP) is a systemic small-vessel vasculitis that is characterized by deposition of IgA antibody immune complexes in different key areas throughout the body. Most often, the condition presents in children with palpable purpura, abdominal pain, and arthritis. When the kidneys are affected, the IgA immune complexes deposit in the glomerulus very similarly to IgA nephropathy and will present in a similar way.{{Cite journal|last1=Kraft|first1=D. M.|last2=Mckee|first2=D.|last3=Scott|first3=C.|date=August 1998|title=Henoch–Schönlein purpura: a review|journal=American Family Physician|volume=58|issue=2|pages=405–408, 411|issn=0002-838X|pmid=9713395}}
• Hemolytic uremic syndrome - Most cases occur immediately following infectious diarrhea caused by a specific type of E. coli (O157:H7). The bacteria produces a toxin that causes widespread inflammation and numerous blood clots in small blood vessels (thrombotic microangiopathy). When the inflammation reaches the kidney, or the by-products of systemic inflammation build up in the kidney, the patient will begin showing signs of nephritic syndrome or potentially acute kidney failure (elevated creatinine, BUN, etc.).{{Cite journal|last1=Cody|first1=Ellen M.|last2=Dixon|first2=Bradley P.|date=February 2019|title=Hemolytic Uremic Syndrome|journal=Pediatric Clinics of North America|volume=66|issue=1|pages=235–246|doi=10.1016/j.pcl.2018.09.011|issn=1557-8240|pmid=30454746|s2cid=53875876 }}

• Goodpasture syndrome - This is a rare autoimmune disease where autoantibodies are produced that target the glomerular basement membrane in both the lungs and the kidneys. The damage to the basement membrane causes bleeding, and the disease often presents in patients as hematuria and haemoptysis (coughing up blood). If not treated promptly with plasmapharesis to remove the autoantibodies, it can lead to permanent damage in the lungs/kidneys.{{Cite journal|last1=Salama|first1=A. D.|last2=Levy|first2=J. B.|last3=Lightstone|first3=L.|last4=Pusey|first4=C. D.|date=2001-09-15|title=Goodpasture's disease|journal=Lancet|volume=358|issue=9285|pages=917–920|doi=10.1016/S0140-6736(01)06077-9|issn=0140-6736|pmid=11567730|s2cid=40175400}}
• Systemic Lupus Erythematosus (SLE) - Better known as simply "Lupus", this autoimmune disease can affect nearly every major system in the human body and the kidneys are no exception. Autoantibodies produced in SLE can form immune complexes that deposit along the glomerular basement membrane and cause glomerular inflammation which leads to a nephritic syndrome.{{Cite journal|last=Ward|first=M. M.|date=2000-11-13|title=Changes in the incidence of end-stage renal disease due to lupus nephritis, 1982-1995|journal=Archives of Internal Medicine|volume=160|issue=20|pages=3136–3140|doi=10.1001/archinte.160.20.3136|issn=0003-9926|pmid=11074743|doi-access=}}
• Rapidly progressive glomerulonephritis - This is a syndrome of the kidney that is characterized by rapid loss of kidney function (usually >50% decline in glomerular filtration rate (GFR) within 3 months){{Cite journal|url=https://emedicine.medscape.com/article/240457-overview|title=Rapidly Progressive Glomerulonephritis|last=Lohr|first=James W.|date=January 10, 2018|website=Medscape|access-date=January 21, 2020}} with glomerular crescent formation frequently seen on kidney biopsy. Without treatment, it will quickly lead to kidney failure and potentially death within months. This syndrome has numerous underlying causes that can also cause nephritic syndrome, so this may be more of an association than a cause.{{Cite journal|last=Bhowmik|first=Dipankar|date=January 2011|title=Clinical Approach to Rapidly Progressive Renal Failure|url=http://www.japi.org/january_2011/oa_%20clinical%20approach.pdf|journal=Journal of the Association of Physicians of India|volume=59|pages=38–44|pmid=21751663}}
• Infective endocarditis - Infection that affects the inner lining of the heart (endocardium) and can potentially cause a thrombus to form on one or more heart valves and, if left untreated, can cause septic emboli that can have many systemic effects, including deposition into the glomerulus, causing glomerulonephritis and nephritic syndrome.{{Cite book|title=Robbins basic pathology|date=2007|publisher=Saunders/Elsevier|others=Kumar, Vinay, 1944-, Robbins, Stanley L. (Stanley Leonard), 1915-2003.|isbn=978-1-4160-2973-1|edition=8th|location=Philadelphia, PA|pages=406–408|oclc=69672074}}
• Cryoglobulinemia - Antibodies that are sensitive to the cold can become activated in cold conditions and cause an increase in blood viscosity (hyperviscosity syndrome) as well as forming immune complexes that can deposit in the small blood vessels and can cause nephritic syndrome when this occurs in the kidneys.{{Cite journal|last1=Retamozo|first1=Soledad|last2=Brito-Zerón|first2=Pilar|last3=Bosch|first3=Xavier|last4=Stone|first4=John H.|last5=Ramos-Casals|first5=Manuel|date=November 2013|title=Cryoglobulinemic disease|journal=Oncology (Williston Park, N.Y.)|volume=27|issue=11|pages=1098–1105, 1110–1116|issn=0890-9091|pmid=24575538}}
• Membranoproliferative glomerulonephritis (MPGN) - Another type of glomerulonephritis that is caused primarily by immune complex deposition in the glomerular mesangium and glomerular basement membrane thickening, which activates the complement cascade and damages the glomerulus. This damage leads to inflammation in the glomerulus and can present with a nephritic syndrome.{{Cite journal|last1=Habib|first1=R.|last2=Gubler|first2=M. C.|last3=Loirat|first3=C.|last4=Mäiz|first4=H. B.|last5=Levy|first5=M.|date=April 1975|title=Dense deposit disease: a variant of membranoproliferative glomerulonephritis|journal=Kidney International|volume=7|issue=4|pages=204–215|doi=10.1038/ki.1975.32|issn=0085-2538|pmid=1095806|doi-access=free}}
• Other ANCA small-vessel vasculitides - The conditions included in this category are eosinophilic granulomatosis with polyangiitis, microscopic polyangiitis, and granulomatosis with polyangiitis.{{Cite book|title=Harrison's principles of internal medicine.|date=2012|publisher=McGraw-Hill|others=Longo, Dan L. (Dan Louis), 1949-, Fauci, Anthony S., 1940-, Kasper, Dennis L., Hauser, Stephen L., Jameson, J. Larry., Loscalzo, Joseph.|isbn=978-0-07-174890-2|edition=18th|location=New York|pages=2334–2345|oclc=747712285}}

The pathophysiology of nephritic syndrome is dependent on the underlying disease process, which can vary depending on what condition the nephritic syndrome is secondary to. More specifically, different diseases (many of which are mentioned above in the Causes section) affect different segments of the glomerulus and cause disease-specific segments of the glomerulus to become inflamed. Most often, it is dependent on what part of the glomerulus is damaged by antibody-antigen complex (immune complex) deposition. In all cases, however, the inflammatory processes in the glomerulus cause the capillaries to swell and the pores between podocytes become large enough that inappropriate contents in the blood plasma (i.e. red blood cells, protein, etc.) will begin to spill into the urine. This causes a decrease in glomerular filtration rate (GFR) and, if left untreated over time, will eventually produce uremic symptoms and retention of sodium and water in the body, leading to both edema and hypertension.

The diagnostic approach to nephritic syndrome includes evaluating the patient for any suspected underlying pathology that could cause a nephritic syndrome.{{citation needed|date=February 2020}}

If the person in the office is being examined by a physician, some physical exam findings consistent with nephritic syndrome include the following:

• Edema - This could present as generalized edema (anasarca) or specific swelling of the hands, feet, and/or face.
• Other signs of fluid overload - Diffuse rales (crackles) may be heard at bilateral lung bases or diffusely in all lung fields on auscultation with a stethoscope. Jugular venous distention (JVD) may also be appreciated when visualizing the veins of the neck on physical exam.
• Elevated blood pressure - Measured at least two separate times with at least two minutes between measurements using a sphygmomanometer or equivalent method.{{Cite web|url=http://www.nhlbi.nih.gov/hbp/detect/tips.htm|title=Tips for having your blood pressure taken|date=July 2, 2014|website=National Heart, Lung, and Blood Institute|url-status=dead|archive-url=https://web.archive.org/web/20140702221540/http://www.nhlbi.nih.gov/hbp/detect/tips.htm|archive-date=July 2, 2014}}
• Abnormal heart sounds - If the underlying cause is cardiac in nature (such as infective endocarditis), then you may appreciate abnormal heart sounds during auscultation of the heart.{{Cite web|url=https://depts.washington.edu/physdx/heart/tech2.html|title=Techniques: Heart Sounds & Murmurs|website=University of Washington Department of Medicine|access-date=January 22, 2020}}

If the physician is suspicious of a possible nephritic syndrome, then he/she may order some common lab tests including:

• Serum electrolytes - The kidney is one of the main regulators of electrolytes in the human body and measuring the different electrolyte levels using either a basic metabolic panel (BMP) or comprehensive metabolic panel (CMP) can be a useful indicator of the underlying pathology.{{Cite web|url=https://medlineplus.gov/ency/article/002350.htm|title=Electrolytes|date=November 20, 2017|website=MedlinePlus|access-date=January 22, 2020}}
• Serum creatinine - Also measured using a BMP or CMP, creatinine is one of the most important indicators of current kidney function and is used to calculate the glomerular filtration rate (GFR). An elevated creatinine level is considered abnormal and may indicate decreased kidney function.{{Cite web|url=https://medlineplus.gov/ency/article/003475.htm|title=Creatinine Blood Test|date=July 15, 2017|website=MedlinePlus|access-date=January 22, 2020}}
• Blood urea nitrogen (BUN) - Also measured using a BMP or CMP, blood urea nitrogen is an indicator of how much nitrogen is in the blood at the time of the phlebotomy. The kidney is responsible for excreting nitrogenous substances in the urine, so an elevated BUN usually indicates that the kidney is not functioning appropriately.{{Cite web|url=https://medlineplus.gov/ency/article/003474.htm|title=BUN - blood test|date=April 29, 2019|website=MedlinePlus|access-date=January 22, 2020}}
• Urinalysis - After the patient provides a urine specimen, it is sent to the lab for analysis using a variety of methods including urine dipstick testing and microscopic examination. Because the kidney is responsible for making urine, analyzing the urine directly can provide crucial data that can help the physician diagnose nephritic syndrome.{{Cite web|url=https://medlineplus.gov/ency/article/003579.htm|title=Urinalysis|date=February 7, 2019|website=MedlinePlus|access-date=January 22, 2020}} Some findings on urinalysis that are consistent with nephritic syndrome include red blood cells (hematuria), red blood cell casts, proteinuria, and possibly white blood cells (pyuria).

If nephritic syndrome is identified and diagnosed, then it is important for the physician to determine the underlying cause. To do this, he/she may order any of a large variety of relevant lab tests, some of which are included here:

• Blood culture - This is the process where a sample of the patient's blood is sent to the microbiology lab to attempt to isolate and grow any bacteria that may be circulating in the blood, in order to identify the pathogen.{{Cite journal|last1=Lee|first1=Andrew|last2=Mirrett|first2=Stanley|last3=Reller|first3=L. Barth|last4=Weinstein|first4=Melvin P.|date=November 2007|title=Detection of bloodstream infections in adults: how many blood cultures are needed?|journal=Journal of Clinical Microbiology|volume=45|issue=11|pages=3546–3548|doi=10.1128/JCM.01555-07|issn=0095-1137|pmc=2168497|pmid=17881544}} This is helpful if the physician suspects infection as the underlying cause of the nephritic syndrome.{{cn|date=January 2021}}
• Antinuclear antibody (ANA) titer - ANA is commonly positive in patients who have an underlying autoimmune disease, so this test is useful if the physician suspects an underlying autoimmune disease (refer to the Causes section above for examples) as the cause of the presenting nephritic syndrome. If positive, then the physician may order additional tests to determine which autoimmune condition is the cause and how best to treat it.{{Cite journal|last1=Kavanaugh|first1=A.|last2=Tomar|first2=R.|last3=Reveille|first3=J.|last4=Solomon|first4=D. H.|last5=Homburger|first5=H. A.|date=January 2000|title=Guidelines for clinical use of the antinuclear antibody test and tests for specific autoantibodies to nuclear antigens.|journal=Archives of Pathology & Laboratory Medicine|volume=124|issue=1|pages=71–81|doi=10.5858/2000-124-0071-GFCUOT | url=https://www.archivesofpathology.org/doi/full/10.1043/0003-9985%282000%29124%3C0071%3AGFCUOT%3E2.0.CO%3B2|issn=0003-9985|pmid=10629135|url-access=subscription}}
• Antiglomerular basement membrane (anti-GBM) antibody - If positive, this is highly indicative of Goodpasture's syndrome and can be used to guide treatment.
• Antineutrophil cytoplasmic antibody (ANCA) - If positive, this indicates that there is likely an underlying vasculitis that may be causing the acute nephritic syndrome.{{Cite book|title=Advanced atlas of autoantibody patterns|last=Bradwell, A. R.|date=1999|publisher=The Binding Site|others=Mead, G. P., Stokes, R. P., Binding Site Limited.|isbn=0-7044-8510-9|location=Birmingham|oclc=41258931}}
• Serum complement (C3 and C4) - Complement factors bind to antibodies to form immune complexes and a decreased serum complement level could indicate that the complement is being consumed at a higher rate due to the formation of immune complexes leading to deposition in the glomerulus of the kidney.

A kidney biopsy will provide a fully definitive diagnosis of nephritic syndrome and may also reveal the underlying cause of the nephritic syndrome depending on the underlying pathological process. On biopsy, a patient with nephritic syndrome would show inflammation of numerous glomeruli.{{Cite web|url=https://medlineplus.gov/ency/article/000495.htm|title=Acute nephritic syndrome|date=July 16, 2019|website=MedlinePlus|access-date=January 22, 2020}}

When a patient is confirmed to have nephritic syndrome, the main goal of treatment (regardless of the underlying cause) is to control elevated blood pressures and reduce active inflammation in the kidney itself. Most often, the patient will need to be admitted to the hospital for close monitoring to ensure the efficacy of treatment and make adjustments as needed. Some treatment modalities commonly used to meet these goals include:

• Bed rest during the recovery process to ensure administration of optimal medical therapy with as low of a risk as possible for any exacerbating factors (falls, infection, etc.).{{Cite journal|last1=Allen|first1=C.|last2=Glasziou|first2=P.|last3=Del Mar|first3=C.|date=1999-10-09|title=Bed rest: a potentially harmful treatment needing more careful evaluation|journal=Lancet|volume=354|issue=9186|pages=1229–1233|doi=10.1016/s0140-6736(98)10063-6|issn=0140-6736|pmid=10520630|s2cid=12196831}}
• Fluid restriction to minimize the risk of edema (if not already present) or to reduce any active edema that may be present.{{Cite web|url=https://intermountainphysician.org/_layouts/Custom/KnowledgeRepository/KrDocumentFetch.aspx?target=document&ncid=520429033&tfrm=default|title=Fluid Restricted Diet|date=2016|website=Intermountain Healthcare|access-date=January 23, 2020}}
• A special diet during the hospital stay that restricts sodium, potassium, and fluids in conjunction with the previously mentioned fluid restriction in an attempt to control symptoms of fluid overload.{{Cite journal|last1=Mahtani|first1=Kamal R.|last2=Heneghan|first2=Carl|last3=Onakpoya|first3=Igho|last4=Tierney|first4=Stephanie|last5=Aronson|first5=Jeffrey K.|last6=Roberts|first6=Nia|last7=Hobbs|first7=F. D. Richard|last8=Nunan|first8=David|date=December 1, 2018|title=Reduced Salt Intake for Heart Failure: A Systematic Review|journal=JAMA Internal Medicine|volume=178|issue=12|pages=1693–1700|doi=10.1001/jamainternmed.2018.4673|issn=2168-6114|pmid=30398532|s2cid=53241717|pmc=6422065}}
• Administration of diuretics if patient is showing signs of fluid overload. This will cause excess fluids to be excreted in the urine and may lessen the workload placed on the kidney, allowing it to recover from the inflammatory damage.{{Cite journal|last1=Ali|first1=Syed Salman|last2=Sharma|first2=Pramod Kumar|last3=Garg|first3=Vipin Kumar|last4=Singh|first4=Avnesh Kumar|last5=Mondal|first5=Sambhu Charan|date=April 2012|title=The target-specific transporter and current status of diuretics as antihypertensive|journal=Fundamental & Clinical Pharmacology|volume=26|issue=2|pages=175–179|doi=10.1111/j.1472-8206.2011.01012.x|issn=1472-8206|pmid=22145583|s2cid=43171023}}
• Administration of antihypertensives to alleviate hypertension and maintain a normal blood pressure during the recovery process.{{Cite journal|last1=Wright|first1=Jackson T.|last2=Bakris|first2=George|last3=Greene|first3=Tom|last4=Agodoa|first4=Larry Y.|last5=Appel|first5=Lawrence J.|last6=Charleston|first6=Jeanne|last7=Cheek|first7=DeAnna|last8=Douglas-Baltimore|first8=Janice G.|last9=Gassman|first9=Jennifer|last10=Glassock|first10=Richard|last11=Hebert|first11=Lee|date=2002-11-20|title=Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: results from the AASK trial|journal=JAMA|volume=288|issue=19|pages=2421–2431|doi=10.1001/jama.288.19.2421|issn=0098-7484|pmid=12435255|doi-access=}}
• Administration of anti-inflammatory medications (such as steroids or NSAIDs) to reduce active inflammation in the kidney.{{Cite journal|last1=Rhen|first1=Turk|last2=Cidlowski|first2=John A.|date=2005-10-20|title=Antiinflammatory action of glucocorticoids--new mechanisms for old drugs|journal=The New England Journal of Medicine|volume=353|issue=16|pages=1711–1723|doi=10.1056/NEJMra050541|issn=1533-4406|pmid=16236742|s2cid=5744727 }}
• If the patient is showing signs of kidney failure or end-organ damage, the treatment team may opt to utilize kidney dialysis temporarily (or permanently, in some severe cases) to decrease stress on the kidneys and allow for optimal recovery.{{Cite journal|last1=Tattersall|first1=James|last2=Dekker|first2=Friedo|last3=Heimbürger|first3=Olof|last4=Jager|first4=Kitty J.|last5=Lameire|first5=Norbert|last6=Lindley|first6=Elizabeth|last7=Van Biesen|first7=Wim|last8=Vanholder|first8=Raymond|last9=Zoccali|first9=Carmine|last10=ERBP Advisory Board|date=July 2011|title=When to start dialysis: updated guidance following publication of the Initiating Dialysis Early and Late (IDEAL) study|journal=Nephrology, Dialysis, Transplantation|volume=26|issue=7|pages=2082–2086|doi=10.1093/ndt/gfr168|issn=1460-2385|pmid=21551086|doi-access=}}

Once the acute phase of the nephritic syndrome is controlled, it is crucial to determine the underlying pathology that caused the onset of the acute nephritic syndrome and to treat that condition. If the underlying cause is not determined and treated appropriately, it increases the risk of a recurrence of nephritic syndrome or chronic kidney disease (CKD) in the future.

Because nephritic syndrome is a syndrome and not a disease, the prognosis depends on the underlying cause. Generally, the prognosis of nephritic syndrome in children is better than it is in adults.{{Cite web|title = Acute Nephritis; Nephrosis; Nephritic syndrome information. Patient {{!}} Patient|url = http://patient.info/doctor/acute-nephritis-and-nephrosis|website = Patient|access-date = 2015-10-27|language = en-GB}}

According to the CDC, nephritis/nephrosis/nephritic syndrome was the 9th leading cause of death in the United States in 2017.{{Cite web|url=https://www.cdc.gov/nchs/data/hus/2018/006.pdf|title=Leading causes of death and numbers of deaths, by sex, race, and Hispanic origin: United States, 1980 and 2017|date=2018|website=CDC|access-date=January 21, 2020}} It was listed as the cause of death for 50,633 out of the total 2,813,503 deaths reported in 2017.

The southeast region of the United States reported a significantly higher death rate due to kidney disease than any other region in 2017. Mississippi reported the highest death rate due to kidney disease (21.7), followed by Louisiana (20.6) and Arkansas (19.7).{{Cite web|url=https://www.cdc.gov/nchs/pressroom/sosmap/kidney_disease_mortality/kidney_disease.htm|title=Kidney Disease Mortality by State|date=2017|website=CDC|access-date=January 21, 2020}} Although Vermont reported the lowest death rate due to kidney disease (3.3), the western United States reported the lowest regional average death rate due to kidney disease in 2017.

Out of the 1,374,392 female deaths reported in the US in 2017, kidney disease was listed as the cause of death for 24,889 women and was reported as the 9th overall cause of death for women in 2017.

Out of the 1,439,111 male deaths reported in the US in 2017, kidney disease was not listed in the top 10 causes of death.

Out of the 2,378,385 deaths reported in individuals who identified as White, kidney disease was ranked 10th overall (39,105 deaths) in causes of death in the US in 2017.

Out of the 340,644 deaths reported in individuals who identified as Black or African American, kidney disease was ranked 8th overall (9,609 deaths) in causes of death in the US in 2017.

Out of the 74,094 deaths reported in individuals who identified as Asian or Pacific Islander, kidney disease was ranked 9th overall (1,563 deaths) in causes of death in the US in 2017.

Out of the 197,249 deaths reported in individuals who identified as Hispanic or Latino, kidney disease was ranked 10th overall (3,928 deaths) in causes of death in the US 2017.

In a review of Romanian cases, a 10-year review yielded that upon biopsy, nephritic syndrome was the second most common clinical syndrome at 21.9% (nephrotic syndrome was 52.3%){{cite journal |last1=Covic |first1=Adrian |last2=Schiller |first2=Adalbert |last3=Volovat |first3=Carmen |last4=Gluhovschi |first4=Gheorghe |last5=Gusbeth-Tatomir |first5=Paul |last6=Petrica |first6=Ligia |last7=Caruntu |first7=Irina-Draga |last8=Bozdog |first8=Gheorghe |last9=Velciov |first9=Silvia |last10=Trandafirescu |first10=Virginia |last11=Bob |first11=Flaviu |last12=Gluhovschi |first12=Cristina |title=Epidemiology of renal disease in Romania: a 10 year review of two regional renal biopsy databases |journal=Nephrology Dialysis Transplantation |date=1 February 2006 |volume=21 |issue=2 |pages=419–424 |doi=10.1093/ndt/gfi207 |pmid=16249204 |url=https://academic.oup.com/ndt/article/21/2/419/1850709 |access-date=1 May 2020 |language=en |issn=0931-0509|doi-access=free |url-access=subscription }}

{{Reflist|32em}}

• {{Cite book|title = Pathophysiology|url = https://books.google.com/books?id=5WVCE4JUCQUC|publisher = Jones & Bartlett Learning|date = 2002-01-01|isbn = 9781556425653|first1 = Eileen M.|last1 = Crutchlow|first2 = Pamela J.|last2 = Dudac|first3 = Suzanne|last3 = MacAvoy|first4 = Bernadette R.|last4 = Madara}}
• {{Cite book|title = Manual of Nephrology|url = https://books.google.com/books?id=J9CQAwAAQBAJ|publisher = Lippincott Williams & Wilkins|date = 2014-05-13|isbn = 9781469887364|first = Robert W.|last = Schrier}}

{{Medical resources

| DiseasesDB =

| ICD10 = {{ICD10|N|00||n|00}}, {{ICD10|N|01||n|00}}, {{ICD10|N|03||n|00}}, {{ICD10|N|05||n|00}}

| ICD9 = {{ICD9|580}}

| ICDO =

| OMIM =

| MedlinePlus = 000495

| eMedicineSubj =

| eMedicineTopic =

| MeshID =

}}

{{Commons}}

{{Scholia|topic}}

{{Nephrology}}

{{Medicine}}

Category:Glomerular diseases

Category:Syndromes affecting the kidneys