Nephritic syndrome

7 Interesting Facts of Nephritic syndrome

  • Nephritic syndrome is a clinical manifestation of glomerulonephritis, characterized by hematuria, proteinuria, impaired renal function, hypertension, and edema
  • Causative diseases include infection (especially streptococcal upper respiratory infection), IgA glomerulopathy, IgA vasculitis (Henoch-Schönlein purpura), and anti–glomerular basement membrane disease
  • Initial diagnosis can be established based on urinalysis (including sediment examination), serum chemistry profile, and physical examination findings, including blood pressure measurements
  • Renal biopsy is the gold standard for confirming diagnosis of nephritic syndrome and plays an important role in guiding treatment
  • Treatment includes general measures to support kidney function and prevent progression of renal dysfunction, as well as disease-specific treatment
    • General measures can include diuretics, ACE inhibitors or angiotensin receptor agonists, and dialysis
    • For conditions due to production of autoantibodies (antineutrophil cytoplasmic antibody–associated vasculitis, lupus, anti–glomerular basement membrane disease), immunosuppressants are used; plasmapheresis may be required initially to reduce levels of the autoantibody
    • Steroids, with or without cyclophosphamide, are indicated in IgA nephropathy with persistent proteinuria or rapid progression and extensive crescent formation on biopsy
    • Appropriate antimicrobials are given in infection-related cases
  • Complications include rapidly progressive glomerulonephritis, acute and chronic renal failure, pulmonary edema, and hypertensive encephalopathy
  • Prognosis depends on underlying cause; for streptococcal glomerulonephritis, prognosis is typically good in children but may be associated with 20% to 25% mortality in older adults 


  • Treatment success is relative, with a high risk of recurrence in some conditions (eg, lupus, IgA nephropathy)

Nephritic syndrome is a manifestation of glomerulonephritis consisting of a constellation of clinical and laboratory findings, including: 

Hematuria: microscopic with RBCs, typically dysmorphic (glomerular hematuria); RBC casts may be present


Impaired renal function (eg, fluid retention, edema)

Proteinuria may or may not be present

Mild to moderate when present, usually less than nephrotic range (ie, less than 3.5 g/24 hours)

Nephritic syndrome occurs as a spectrum from mild (eg, microscopic hematuria, proteinuria) to severe (eg, oliguria, anuria, hypertension); causes are varied and may include autoimmune, infectious, and hereditary conditions 

Glomerulonephritis includes a group of conditions in which the basic underlying problem relates to injury in the glomerulus (the renal filtering unit); glomerulonephritis may also present as nephrotic syndrome 


  • Nephritic syndrome is 1 manifestation within overall classification of glomerular disease based on pattern of clinical presentation 
    • Nephritic syndrome
      • Occurs as a result of glomerular injury secondary to an inflammatory response within glomeruli
      • Defined by presence of macroscopic or microscopic hematuria (sometimes with RBC casts), sub–nephrotic range proteinuria, hypertension, and oliguria
      • Usually presents over the course of several days with diminished urine output, weight gain, edema, and hypertension
    • Nephrotic syndrome
      • Results from structural damage to glomerular filtration barrier, leading to increased permeability of capillary wall to protein
      • Defined by presence of heavy proteinuria (greater than 3.5 g/day), hypoalbuminemia (less than 3 g/dL), peripheral edema, and hypercholesterolemia 
      • Usually presents with insidious onset of edema, except in minimal change disease, which is characterized by sudden onset of edema
      • Associated with hypercoagulable state with risk for venous and arterial thrombotic events and increased risk for infection (due to urinary loss of proteins and immunoglobulins)
      • Many causes eventually lead to chronic progressive renal failure
    • Rapidly progressive glomerulonephritis
      • Glomerulonephritis leading to rapidly progressive renal failure, usually associated with nephritic urinary sediment (sub–nephrotic range proteinuria, hematuria with RBC casts); may have elevated blood pressure
    • Chronic glomerulonephritis
      • Slowly progressive condition associated with hypertension, edema, mild to moderate proteinuria, abnormal urine sediment, and gradual decline in renal function and size of kidneys
      • Often associated with development of secondary hyperparathyroidism, normochromic normocytic anemia, and mild metabolic acidosis
Typical featuresNephritic syndromeNephrotic syndrome
Manifestation of glomerular injuryGlomerular inflammation results in reduced GFR, nonnephrotic proteinuria, mild edema and hypertension (secondary to sodium retention), and hematuria with RBC castsStructural damage to glomerular filtration barrier leads to increased permeability of capillary wall to protein, resulting in massive protein loss in the urine, hypoalbuminemia, lipiduria, hypercholesterolemia, and massive edema
Edema++++++ (secondary to hypoalbuminemia, and salt and water retention)
Blood pressureElevatedTypically within reference limits; may be decreased or elevated
Hematuria+++ (prominent)+/- (few)
Urine castsRBC casts presentFatty casts may be present
Urine qualityMicroscopic hematuria; oliguriaMay be frothy
Proteinuria+/- (variable)++++ (greater than 3-3.5 g/day)
GFRDecreasedUsually not decreased early in course
Renal insufficiencyCommon at presentationUncommon at presentation
Serum albuminWithin reference limits or slightly raisedLow 
Common underlying conditionsPoststreptococcal glomerulonephritis and other postinfectious processes
Infection-related processes (endocarditis-abscess-shunt) 
IgA nephropathy (Berger disease)
Antineutrophil cytoplasmic antibody–associated vasculitis
Lupus nephritis
IgA vasculitis (Henoch-Schönlein purpura)
Anti–glomerular basement membrane antibody
Minimal change disease
Diabetic nephropathy
Focal segmental glomerulosclerosis
Membranous nephropathy
Amyloid disease
Dense deposit disease
TreatmentAddress underlying cause Diuretics
Antiproteinuric agents
Cholesterol-lowering agents
Sometimes anticoagulants
Address underlying cause
Possible complicationsFluid retention and development of severe hypertension may lead to pulmonary and cerebral edemaInfection secondary to urinary loss of immunoglobulins
Hypercoagulable state with risk for venous and arterial thromboembolism
Prolonged nephrotic syndrome may lead to progressive renal failure
Acute renal failure may result from volume depletion
Renal vein thrombosis
Adverse drug reaction
PrognosisDepends on cause      Relapsing or chronic condition for many patients, depending on cause and response to specific therapy

Caption: NOTE: Some glomerular diseases may present with either a nephritic or nephrotic syndrome (eg, membranoproliferative glomerulonephritis).

Citation: Adapted from Floege J et al: Introduction to glomerular disease: clinical presentations. In: Feehally J et al, eds: Comprehensive Clinical Nephrology. 6th ed. Elsevier; 2019: 184-98.e1, Table 15.4 and Radhakrishnan J et al: Glomerular disorders and nephrotic syndromes. In: Goldman L et al, eds: Goldman-Cecil Medicine. 26th ed. Elsevier; 2020:753-63.e2, Table 113-1. Data from Mathieson P: Primary glomerular disease. Medicine. 47(10):636-43, 2019; Conway B et al: Nephrology and urology. In: Ralston SH et al, eds: Davidson’s Principles and Practice of Medicine. 23rd ed. Elsevier; 2018:381-440; and Khanna R: Clinical presentation & management of glomerular diseases: hematuria, nephritic & nephrotic syndrome. Mo Med. 108(1):33-6, 2011.


  • Onset of illness is generally fairly abrupt, evolving over several days
  • General symptoms
    • Hematuria
      • Macroscopic hematuria, when present, is often the symptom for which the patient seeks medical evaluation
        • May be red, but more commonly described as rusty, tea-, or cola-colored
        • Painless
      • May be microscopic and therefore unrecognized
    • Oliguria
    • Fluid retention may cause swelling of face and legs, dyspnea, abdominal pain, and weight gain
    • Headache is common and may relate to hypertension
    • Other nonspecific symptoms may be present (eg, generalized fatigue, malaise)
    • Rapidly progressive glomerulonephritis may culminate in uremia and/or hypertensive encephalopathy, with symptoms of nausea, vomiting, pruritus, altered mental status, and seizures
  • Some patients are asymptomatic or have nonspecific complaints (eg, fatigue, weakness, nausea)
  • Other medical history (chronic medical conditions) may support diagnosis and/or suggest cause:
    • Recent pharyngitis or skin infection approximately 1.5 to 3 weeks before onset of hematuria in children (poststreptococcal glomerulonephritis) 
    • Subacute or chronic infection (eg, osteomyelitis, endocarditis, visceral abscess, shunt infection, hepatitis B or C) may also be complicated by glomerulonephritis presenting with nephritic syndrome
    • Single or recurring episodes of hematuria 1 to 3 days after onset of an upper respiratory tract infection (IgA nephropathy) 
    • Concurrent rash, arthralgias/arthritis, and gastrointestinal symptoms (IgA vasculitis, formerly Henoch-Schönlein purpura)
    • Malar rash, photosensitivity, mucosal ulcerations, alopecia, arthritis, myalgias, and constitutional symptoms (systemic lupus erythematosus)
    • Cough, dyspnea, recurrent noninfectious sinusitis, hemoptysis, pulmonary hemorrhage (anti–glomerular basement membrane disease [Goodpasture syndrome], granulomatosis with polyangiitis [Wegener granulomatosis])
    • Lymphoma may precipitate membranoproliferative disease presenting with nephritic syndrome
    • Some medications (eg, propylthiouracil, allopurinol, hydralazine) have been implicated as triggers of autoimmune vasculitis and glomerulonephritis with a nephritic presentation

Physical examination

  • Findings associated with nephritic syndrome:
    • High blood pressure is a hallmark of nephritis 
    • Additional signs of fluid overload
      • Weight gain
      • Nonpitting edema
        • Puffy eyelids and facial edema, especially in the morning, before or shortly after arising 
        • Peripheral edema 
      • Jugular venous distention
      • Rales, decreased breath sounds, and dullness to percussion of chest
    • Flank tenderness may be elicited on percussion
  • Other findings may suggest an underlying or precipitating condition
    • Palpable purpura, skin or mucosal ulcerations, episcleritis/scleritis, peripheral neuropathy in systemic vasculitic conditions; IgA vasculitis lesions are often most prominent on the legs, lower abdomen, and buttocks
    • Malar rash, alopecia, and mucosal ulcerations in systemic lupus erythematosus
    • Purpura, acrocyanosis, and acral ulcerations with cryoglobulinemia
    • Draining sinus tract may be present in osteomyelitis
    • New or prominent cardiac murmur and typical stigmata (eg, Roth spots, conjunctival petechiae, splinter hemorrhages, Janeway lesions) suggest endocarditis
    • Prominent, diffuse lymphadenopathy, and splenomegaly may be palpable in patients with lymphoma


  • Nephritic syndrome is the presenting manifestation of some forms of glomerulonephritis
    • Glomerular inflammation may occur through several mechanisms; certain diseases are attributed to each of these causes, but overlap (multiple mechanisms) occurs in some cases
      • Immune complex–mediated
        • IgA nephropathy (also referred to as Berger disease
          • Most common form of chronic glomerulonephritis; characterized by a variable course usually associated with a relentless decline in renal function 
          • Presents with recurrent macroscopic hematuria (often associated with concurrent upper respiratory tract infection) with intervening episodes of microscopic hematuria and/or mild proteinuria 
          • Characterized by diffuse glomerular IgA (particularly IgA1 subclass) deposits 
        • Henoch-Schönlein purpura
          • Systemic IgA vasculitis with renal manifestations that commonly presents in pediatric population
          • Often self-limiting process in children; may result in chronic or progressive renal dysfunction in adults
          • Classically presents with a combination of palpable purpura, arthralgia, abdominal pain, and renal disease
          • Nephritis associated with IgA vasculitis is characterized by diffuse glomerular fibrin and IgA deposits with greater frequency of severe lesions (eg, crescents, necrosis) compared with IgA nephropathy 
        • Infection-associated glomerulonephropathy
          • Immune complex formation in response to infection, with deposition of complexes in glomeruli 
          • Postinfectious glomerulonephropathy is classically associated with group A streptococcal infection (upper respiratory tract or dermal), but more recently has been linked with other pathogens and conditions (Related: Poststreptococcal glomerulonephritis)
          • May occur concurrently with deep-seated infections (eg, endocarditis, osteomyelitis, visceral abscess, ventriculoatrial shunt infections)
          • Bacterial, viral, fungal, and parasitic pathogens have been associated
        • Systemic lupus erythematosus
          • Renal disease results from deposition of immune complexes involving the autoantibodies associated with systemic lupus erythematosus (eg, antinuclear antibodies, double-stranded DNA antibodies) 
          • Nephritic syndrome usually occurs within 5 years of lupus onset; may be first manifestation that leads to lupus diagnosis 
      • Vasculitis (pauci-immune-mediated)
        • Primarily small-vessel, usually antineutrophil cytoplasmic antibodies (ANCA)–positive
          • Most common cause of rapidly progressive glomerulonephritis 
          • Certain medications (eg, propylthiouracil, allopurinol, hydralazine) may trigger antineutrophil cytoplasmic antibody formation
          • Granulomatosis with polyangiitis (previously referred to as Wegener granulomatosis
            • Rare multisystem autoimmune disease characterized by inflammatory changes in sinuses, lungs, and kidneys
          • Eosinophilic granulomatosis with polyangiitis (previously referred to as Churg-Strauss syndrome
            • Rare multisystem autoimmune disease characterized by disseminated necrotizing vasculitis; occurs among patients with asthma and tissue eosinophilia
      • Anti–glomerular basement membrane disease 
        • Rare autoimmune disorder characterized by small-vessel vasculitis that can affect both glomerular and pulmonary capillaries
        • Sometimes referred to as Goodpasture syndrome when clinical manifestation includes both glomerulonephritis and pulmonary hemorrhage
      • Hereditary nephritis (Alport syndrome)
        • Structural defect in glomerular basement membrane caused by type IV collagen gene mutations (either the COL4A3 or COL4A4 [OMIM # 203780] or the COL4A5 [OMIM # 301050]); X-linked transmission is most common, but autosomal recessive inheritance is possible
        • Characterized by glomerulonephritis associated with hematuria and proteinuria presenting in a nephritic pattern, along with high-pitched hearing loss and abnormalities of the lens of the eye (lenticonus) 
        • When present, family history of disease and/or deafness may be sufficient to make diagnosis; genetic testing may provide supporting evidence
        • Confirm diagnosis by characteristic biopsy (defects in the glomerular basement membrane without inflammation) and electron microscopy findings (areas of glomerular basement membrane thinning and other areas of glomerular basement membrane splitting with lamellations)

Risk factors and/or associations

  • Some underlying diseases that can lead to nephritic syndrome have a higher incidence in certain age groups:
    • Incidence of anti–glomerular basement membrane disease peaks in the third, sixth, and seventh decades of life 
    • IgA nephropathy more commonly presents in children and young adults 
    • IgA vasculitis (Henoch-Schönlein purpura) is more common in children than in adults 
    • Poststreptococcal glomerulonephritis
      • Most common in children between ages 2 and 6 years with a history of pharyngitis or pyoderma 
      • Epidemiology has been shifting in past 3 decades; in developed countries, it is now more common in the older adult populations 
  • In young adults, anti–glomerular basement membrane disease is more common in men than in women 
  • Postinfectious glomerulonephritis is reported more often in males than in females among both children and adults 
  • IgA nephropathy occurs more commonly in males than females 
  • Familial pattern of inheritance for Alport syndrome may be noted (X-linked recessive or autosomal recessive) depending on pathologic variant 
  • IgA nephropathy is thought to have a genetic predisposition; a mutation at 6q22-q23 has been identified and others are postulated

How is Nephritic syndrome Diagnosed?

  • Diagnosis is suggested by clinical presentation; most common presenting patterns include:
    • Symptomatic: dark urine, low urine volume, hypertension, and fluid retention with edema
    • Asymptomatic: abnormal urine sediment on routine laboratory testing in patient without other clinical manifestations
  • Urinalysis with urine microscopy is the essential first step
    • Nephritic urine sediment is characterized by more than 5 RBCs/high-power field with presence of 1 or more of the following: acanthocytes, red cell casts or mixed red cell/white cell casts; nephrotic range proteinuria is usually absent 
  • Assess renal function with serum creatinine, BUN, and creatinine clearance levels 
  • Initial laboratory tests should include electrolytes, complement levels (CH50, C3, C4), CBC, and liver function tests 
  • Other tests may be directed at likely underlying causes based on patient age and clinical presentation (eg, antinuclear antibodies, anti-DNA, antineutrophil cytoplasmic antibodies, anti–glomerular basement membrane, antistreptolysin O titer, cryoglobulins, hepatitis B and C serologies, HIV test, blood cultures) 
  • Imaging aids in assessing chronicity and prognosis, determining advisability of renal biopsy, and excluding alternate diagnosis 
  • Renal biopsy is the gold standard for diagnosing underlying cause of nephritic syndrome and generally plays an important role in guiding treatment; however, disagreement exists regarding the uniform necessity of renal biopsy, and decisions should be individualized in consultation with a nephrologist
    • KDIGO (Kidney Disease: Improving Global Outcomes) guidelines recommend it for all cases of nephritic presentation 
    • Other experts suggest that patients with normal blood pressure and renal function and minimal proteinuria do not require kidney biopsy, especially if other clinical circumstances suggest a diagnosis with a clear treatment strategy (eg, infection-associated), reserving biopsy for unclear diagnosis and/or abnormal kidney function 
    • Biopsy of another site may also establish diagnosis (eg, skin lesions for IgA vasculitis) and obviate need for renal biopsy 


  • Urinalysis
    • Normal urine sediment usually contains fewer than 2 RBCs/high-power field and dysmorphic RBCs (acanthocytes) are generally absent; urine dipstick for blood is usually negative (trace may be noted in some patients without disease) 
    • Specific findings include:
      • Hematuria 
        • May be macroscopic or microscopic 
        • RBC casts and dysmorphic RBCs (acanthocytes) are hallmarks of nephritis 
      • Proteinuria
        • May be detected on dipstick but should be quantified by 24-hour urine collection; a spot urine protein (or albumin) to creatinine ratio is an alternative to a 24-hour collection 
        • 24-hour urine collection: results in patients with nephritic syndrome may exceed reference range, but are usually subnephrotic (less than 3.5 g/day) 
          • 24-hour creatinine should be measured in conjunction to assess completeness of collection by comparing against reference values 
      • Hyaline casts and/or pyuria with leukocytes and WBC casts may also be present 
  • Complement 
    • Low serum complement levels are seen in some diseases associated with nephritic syndrome and indicate a need for further evaluation; pattern may suggest specific diagnosis
      • Low C3 level with low or normal C4 level occurs in glomerulonephritis associated with infections 
      • Low C3 and C4 levels are seen in some cases of lupus nephritis, membranoproliferative glomerulonephritis (type 1), cryoglobulinemia, and glomerulonephritis associated with hepatitis C 
      • CH50 is usually low in disease states such as lupus nephritis, cryoglobulinemia, poststreptococcal glomerulonephritis, membranoproliferative glomerulonephritis (type 1), poststreptococcal glomerulonephritis, and glomerulonephritis associated with some other infections (eg, endocarditis, shunt nephritis)
    • Complement levels within reference range are typical in antineutrophil cytoplasmic antibody-associated vasculitides, IgA vasculitis, IgA nephropathy, and anti–glomerular basement membrane diseases 
  • Renal function tests and electrolytes
    • Often shows elevated creatinine and BUN levels, but this is not an invariable finding; serum albumin level may be within reference range or slightly low 
  • Creatinine clearance
    • May be measured on a 24-hour specimen or may be estimated mathematically using serum creatinine and patient-specific parameters 
  • Liver function tests
    • May suggest underlying cause (eg, viral hepatitis) or condition (hypoalbuminemia suggesting overlap with nephrotic picture)
  • CBC
    • Anemia may suggest chronicity and significant kidney dysfunction
    • May suggest underlying cause (eg, pyogenic infection)


  • Renal ultrasonography
    • Findings are nonspecific; kidneys may be enlarged with increased echogenicity 
    • Demonstration of small, shrunken kidneys suggests chronic, irreversible disease 
    • May delineate alternative causes for hematuria (eg, renal stones, renal mass)


Renal biopsy 
General explanation
  • Collection of renal tissue for histologic analysis, usually ultrasonography-guided core needle technique
  • Abnormal kidney function with an active urine sediment (eg, dysmorphic RBCs, cellular casts)
  • Unexplained proteinuria
  • Systemic disease with abnormal kidney function, proteinuria, or dysmorphic hematuria
  • Unexplained abnormal renal function
  • Uncontrolled severe hypertension
  • Uncorrected coagulopathy
  • Active renal infection
  • Certain abnormalities of the kidneys and solitary kidney are relative contraindications
Interpretation of results
  • Histologic findings vary based on cause of nephritis; immunohistologic techniques and electron microscopy are often used to augment conventional light microscopy
  • Active inflammatory cells (monocytes, neutrophils) are detected in acute nephritic syndrome
  • Crescentic inflammation of glomeruli is indicative of rapidly progressive nephritis 
  • Chronic changes(eg, fibrosis, tubular atrophy, glomerulosclerosis) are apparent in chronic nephritic syndrome

Differential Diagnosis

Most common

Treatment Goals

  • Delay or stop progression of underlying disease
    • Treat hypertension and proteinuria
    • Treat underlying cause if identified
  • Reduce edema and sequelae of fluid overload
  • Institute renal replacement therapy if needed

Admission criteria

General admission criteria

  • Rapidly progressive glomerulonephritis
  • Oligoanuria
  • Uncontrolled severe hypertension
  • Complications (eg, congestive heart failure)
Criteria for ICU admission
  • Hypertensive encephalopathy
  • Diffuse alveolar hemorrhage (eg, in vasculitic causes)

Recommendations for specialist referral

  • Consult a nephrologist to aid in diagnosis and management; rapidly progressive glomerulonephritis requires urgent management 
  • Consult appropriate specialist for treatment of condition (eg, rheumatologist, infectious disease specialist, hepatologist) for patients in whom an underlying or precipitating disorder is identified

Treatment Options

General measures to support kidney function and prevent progressive deterioration apply regardless of nephritic syndrome cause

  • Use an ACE inhibitor or an angiotensin receptor blocker for management of both hypertension and proteinuria to prevent further progression of kidney disease 
    • For children, the blood pressure goal for both systolic and diastolic readings is the 50th percentile for age, sex, and height
    • For adults, the target blood pressure is 130/80 mm Hg or lower; some experts suggest a target of 125/75 mm Hg if urine protein loss exceeds 1 g/day
    • Specific urine protein targets have been established for some conditions:
      • For IgA nephropathy and IgA vasculitis (Henoch-Schönlein purpura) nephritis: less than 1 g/day/1.73 m² in adults and less than 0.5 g/day/1.73 m² in children
  • Use nifedipine or nicardipine if hypertension is not adequately controlled with ACE inhibition or angiotensin receptor blockade or in hypertensive urgency requiring parenteral therapy 
  • Loop diuretics (eg, furosemide) are the preferred initial treatment in patients with fluid overload 
  • Dialysis may be necessary for complications of fluid overload (eg, congestive heart failure) in patients who do not respond to diuretics or for metabolic derangement related to declining renal function (eg, hyperkalemia, uremia) 
  • Dietary restrictions on salt and fluid intake are recommended to control hypertension and prevent fluid overload 
  • Weight loss and smoking cessation are recommended if applicable (Related: Tobacco use disorder and smoking cessation)
    • Target BMI: 20 to 25 kg/m² 

Condition-specific treatment may be indicated in addition to general renal support measures 

  • Antineutrophil cytoplasmic antibodies–associated vasculitis
    • Treatment is aimed at suppressing antibody production
    • Plasmapheresis may be required for patients with rapidly deteriorating renal function requiring dialysis or pulmonary hemorrhage
  • Anti–glomerular basement membrane disease
    • Urgent treatment is required with the goal of removing circulating antibody by plasmapheresis and suppressing further production
    • Dialysis is often required acutely
  • IgA nephropathy and IgA vasculitis (Henoch-Schönlein purpura) nephritis
    • Except in cases of rapidly progressive (crescentic) glomerulonephritis, specific treatment is instituted only if proteinuria persists after 3 to 6 months of optimal care (including ACE inhibition and/or angiotensin receptor blockade) and if GFR is greater than 50 mL/minute/1.73 m²
    • For patients with rapidly declining renal function and crescent formation, initiate steroids, with or without cyclophosphamide
  • Infection-related glomerulonephritis
    • Treatment of inciting infection is recommended, although renal disease may not reverse even if infection is successfully eradicated
    • Treat bacterial, fungal, and parasitic infections with appropriate antimicrobial agents
    • Although antiretroviral therapy is now recommended for all patients with HIV infection, regardless of immune status, HIV nephropathy is an indication for prompt initiation as treatment helps to preserve kidney function and may reverse existing dysfunction (Related: HIV infection and AIDS in adults)
    • Guideline-specific antiviral therapy for treatment of hepatitis C and kidney disease is available (Related: Hepatitis C)
    • Treat hepatitis B with nucleoside analog or interferon (Related: Hepatitis B)
  • Lupus nephritis
    • All patients with lupus nephritis should receive hydroxychloroquine (generally under guidance of a rheumatologist), unless a contraindication exists
    • Otherwise, treatment depends on class of kidney involvement, which is defined by histopathologic pattern; various immunosuppressive regimens are in use

Drug therapy

  • Antihypertensive/antiproteinuric drugs
    • ACE-inhibitors
      • Captopril
        • Captopril Oral tablet; Adults: The FDA-approved dosage is 25 mg PO 3 times daily.
    • Angiotensin-receptor blockers
      • Losartan
        • Losartan Potassium Oral tablet; Adults: Initially, 50 mg PO once daily; titrate to 100 mg PO once daily based on blood pressure response.
      • Irbesartan
        • Irbesartan Oral tablet; Adults: Initially, 75 mg PO once daily. Titrate as tolerated to target dose of 300 mg/day PO.
    • Calcium channel blocker
      • Nicardipine
        • Nicardipine Hydrochloride Oral capsule; Children† and Adolescents†: 0.5 mg/kg/dose PO every 8 hours.
        • Nicardipine Hydrochloride Oral capsule; Adults: 20 mg PO 3 times daily, initially. Titrate dosage until goal blood pressure is attained; allow at least 3 days between dosage increases. Usual dose: 20 to 40 mg PO 3 times daily.
  • Loop diuretic
    • Furosemide
      • Furosemide Oral tablet; Adults: Initially, 20 to 80 mg PO as a single dose; may repeat dose in 6 to 8 hours. Usual dose: 40 to 120 mg/day. Max: 600 mg/day.

Nondrug and supportive care

  • Dietary restrictions are recommended (eg, salt and fluid intake restrictions)
    • Recommended salt limit is 5 g/day (2 g sodium) 
    • Fluid restriction is often individualized based on daily weight and input/output measurements
  • Renal replacement therapy may be required in some patients 
    • Volume overload that cannot be controlled by pharmacotherapy
    • Severe uremia, acidosis, and hyperkalemia; these indications are not usually present in early stages of nephritic syndrome, but may occur in rapidly progressive glomerulonephritis

Special populations

  • Pregnant patients
    • ACE inhibitors, angiotensin blocking agents, and many immunosuppressants are contraindicated in pregnancy
    • GFR below reference range and uncontrolled proteinuria increase risk of poor maternal and fetal outcomes 


  • During acute phase, closely monitor serum creatinine level, urine output, and proteinuria to establish tempo of progression and response to treatment 
  • Tailor further monitoring to extent of renal dysfunction, underlying cause, and treatment (eg, immunosuppressants) (Related: Acute kidney injury)
    • May entail follow-up of serum markers of disease (eg, anti–glomerular basement membrane antibodies, antineutrophil cytoplasmic antibody levels) 
      • Drug levels (eg, calcineurin inhibitors used for immunosuppression) 
      • CBC, electrolyte levels, and renal function (eg, BUN and creatinine levels)
    • Repeat biopsy may be indicated for patients who do not respond to therapy 
  • Diseases such as IgA nephropathy, which are lifelong conditions, require regular blood pressure and urine protein monitoring 


  • Complications (eg, encephalopathy, pulmonary edema) from hypertension and fluid retention may occur, usually in the context of rapidly progressive glomerulonephritis
  • Depending on underlying cause, may result in irreversible kidney damage and chronic kidney disease


  • Prognosis depends on underlying cause, patient age, and comorbidities 
    • Antineutrophil cytoplasmic antibody–associated
      • Initial therapy achieves remission in about 80% of patients, but relapses are common 
    • Anti–glomerular basement membrane disease
      • Untreated disease is usually fatal, but plasmapheresis and immunosuppression improve outcomes such that most patients survive 
      • Prompt diagnosis and treatment are essential, as patients who have extensive crescentic pathology are less likely to respond
    • IgA nephropathy
      • Most patients experience steady, progressive disease; 25% to 30% eventually develop chronic kidney dysfunction and end-stage renal disease in 20 to 25 years 
      • Urine protein levels of 1 g/day or more are associated with progressive decline in kidney function, independent of other risk factors 
    • IgA vasculitis (Henoch-Schönlein purpura)
      • Although permanent renal failure is uncommon in all patients with IgA vasculitis, it is more common in those with IgA vasculitis–related nephritic or nephrotic syndrome (about 20%) 
    • Lupus nephritis
      • Disease tends to be progressive in classes III and IV; however, current treatment strategies allow 80% of patients to avoid chronic kidney disease 
    • Infection-associated glomerulonephritis
      • Glomerular inflammation usually improves with successful treatment of infection; however, some degree of kidney dysfunction may remain secondary due to multifactorial nature of renal dysfunction
      • Children: prognosis is typically good 
      • Adults: complete recovery occurs in 40% to 50% of patients and about 10% develop chronic kidney disease 
      • Older adults: chronic kidney disease occurs in about 60% and mortality may reach 20% to 25%


Beck LH Jr et al: Glomerular and tubulointerstitial diseases. Prim Care. 35(2):265-96, vi, 2008 Reference


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