eMedicine Specialties > Nephrology > Glomerular Diseases
Glomerulonephritis, Nonstreptococcal Associated With Infection
Updated: Dec 15, 2008
Introduction
Background
The classic association of glomerulonephritis (GN) with infection is poststreptococcal GN, usually developing after streptococcal pharyngitis (see Glomerulonephritis, Poststreptococcal). However, a number of glomerular diseases are associated with other bacterial, viral, fungal, and parasitic diseases.
Pathophysiology
Most glomerular diseases associated with infection are mediated by the immune complex. The classic example observed in poststreptococcal GN involves an antigen-antibody reaction, which may occur in the circulation or in the glomerulus. Deposition in the glomerulus results in activation of the complement cascade, which may involve either the classic or alternative pathway. The immune complexes may activate endogenous glomerular cells. The reduction of chemotactic factors results in the accumulation of leukocytes and platelets within the glomerulus and, consequently, the inflammatory response.
Several possible pathogenic events occur in viral diseases associated with glomerular injury. These may include the formation of circulating immune complexes involving viral antigens and antibodies, formation of circulating immune complexes induced by the release of antigens following virally induced cellular injury, formation of in situ antigen-antibody reactions or cell-mediated injury, and autoimmune reactions to glomerular structures induced by the virus.
In protozoal infections, such as malaria, antibodies are formed against malarial antigens. The circulating immune complexes activate complement and macrophages. The complexes are primarily deposited in subendothelial areas. A cell-mediated immune response may also occur.
Frequency
United States
The various causes of infection-related GN have different prevalence rates. In endocarditis, associated GN may occur in up to 20% of cases. Staphylococcus aureus has become a more common cause of GN than Streptococcus in developed countries. GN associated with hepatitis C is becoming a far more commonly recognized cause of GN.
International
Although specific numbers for incidence statistics are not available, in certain developing areas of the world, hepatitis B, HIV disease, malaria, and schistosomiasis are major causes of glomerulopathy.
Mortality/Morbidity
Depending on the etiology, the outcome of GN associated with infection can be quite variable.
- In GN associated with bacterial endocarditis, renal function returns after treatment with antibiotics. The GN usually resolves after the infection has cleared, with renal function beginning to improve within 1-2 weeks, complement levels normalizing within 6 weeks, and hematuria normalizing in approximately 6 months.
- The course of GNs associated with viral infection is more variable, although patients with HIV nephropathy commonly progress to end-stage renal disease.
Race
This condition is not limited to any particular race.
Sex
In most GNs associated with infection, no sexual predilection exists. However, HIV-associated GN is far more common in males.
Age
This type of GN can occur at any age.
Clinical
History
Presentation may vary from asymptomatic hematuria to a full-blown acute nephritic syndrome consisting of proteinuria, edema, hypertension, and renal failure.
- Hematuria may be gross or microscopic.
- Patients may have evidence of edema.
- Patients may report fever, night sweats, and rigors.
- Weight loss is a possible complaint.
- Patients may report arthralgias.
- Abdominal, chest, or back pain may be caused by a visceral abscess.
- Patients may have history of shunt placement for hydrocephalus, or they may have a vascular graft that has become infected.
- Patients with hepatitis B or C may have a history of intravenous drug abuse, needle stick injury, blood transfusions, or sexual promiscuity.
- Patients with HIV infection may have history of intravenous drug abuse, hemophilia, history of blood transfusion from 1977-1985, unprotected sex with multiple partners, or tuberculosis.
Physical
- Hypertension may be due to renal failure.
- Edema due to nephrotic syndrome is unusual but can develop in as many as 30% of cases associated with shunt nephritis.
- Rash may be maculopapular or purpuric.
- Lymphadenopathy is a reported finding.
- Patients may have hepatosplenomegaly.
- Findings of subacute bacterial endocarditis (SBE) may include the following:
- Heart murmur
- Purpura
- Roth spots
- Janeway lesions
Causes
Infections with bacteria, viruses, protozoa, and helminths can cause postinfectious GN (PIGN).
- Bacterial endocarditis: PIGN occurs more commonly in subacute rather than acute endocarditis. S aureus is now the most common pathogen recognized.
- Shunt nephritis: This may be associated with ventriculovascular, ventriculoperitoneal, peritoneovascular, or vascular shunts.
- Visceral abscesses: These may occur with abdominal, pulmonary, or retroperitoneal abscesses.
- Syphilis
- Hepatitis B
- Hepatitis C
- Human immunodeficiency virus
- Cytomegalovirus
- Parvovirus B19
- Hantavirus
- Malaria
- Schistosomiasis
- Leishmaniasis
- Filariasis
- Hydatid disease
- Toxoplasmosis
- Aspergillosis
Differential Diagnoses
Glomerulonephritis,
Membranoproliferative
Hemolytic-Uremic Syndrome
IgA Nephropathy
Nephritis, Lupus
Serum Sickness
Other Problems to Be Considered
Type 1 membranoproliferative GN other than that due to infectious causes
Mixed cryoglobulinemia
Atheroembolic disease and hemolytic uremic syndrome: These are examples of nonimmune complex–mediated diseases that may mimic GN.
Workup
Laboratory Studies
- Urinalysis: This may reveal hematuria, pyuria, red blood cell casts, and proteinuria. Findings are very helpful for determining if glomerulonephritis (GN) is primarily of a nephrotic or nephritic type.
- CBC count: The neutrophil count may be elevated in patients with an acute bacterial infection. Eosinophilia may be observed in patients with GN associated with SBE or a parasitic infection. Depending on the duration of disease and severity of renal dysfunction, anemia may be observed due to chronic kidney disease.
- BUN and creatinine: BUN and serum creatinine levels are commonly elevated in patients with infection-related GN. However, levels may be normal early in the course of these disorders.
- Electrolytes: Hyperkalemia or evidence of metabolic acidosis may be observed if the patient presents with chronic renal insufficiency.
- Liver function tests: The aspartate aminotransferase level is commonly elevated in patients with hepatitis-associated GN.
- Rheumatoid factor: The results commonly are positive in patients with GN associated with bacterial endocarditis.
- Serum complement levels (C3, C4, CH50): Complement levels commonly are low in patients with infection-related GN, more so in those with certain diseases. Low complement levels indicate an immune complex disease and are not necessarily diagnostic because they can be present in patients with other immune complex diseases (eg, lupus nephritis).
- Hepatitis panel (hepatitis B surface antigen, hepatitis C antibody): Hepatitis is a common cause of infection-related GN.
- Cryoglobulins: These are commonly present in patients who have GN associated with hepatitis C.
- VDRL test: Findings are positive in patients with GN associated with syphilis.
- HIV testing: This should be performed on all patients with GN and risk factors for HIV infection.
- Viral titers (cytomegalovirus, parvovirus B19, mumps, varicella, Epstein-Barr virus, Hantavirus): Depending on the clinical presentation, drawing blood for viral titers may be important in order to help identify the cause of the GN.
- Stool for ova and parasites: This should be performed if the patient has been in areas endemic to diseases such as schistosomiasis or filariasis.
- Antistreptolysin-O titer, antineutrophil cytoplasmic antibodies, antiglomerular basement membrane antibody, serum protein electrophoresis, and urine protein electrophoresis: Depending on the clinical presentation, these tests may be performed as part of the evaluation to help identify the cause of the GN.
- Other evaluations: In appropriate clinical circumstances, peripheral blood smears to test for malaria may be helpful.
Imaging Studies
- Renal ultrasound: This is routinely obtained in patients presenting with abnormal renal function to help rule out obstructive causes of nephropathy, and findings demonstrate certain anatomic abnormalities. It is also useful to confirm the presence of 2 functioning kidneys prior to performing percutaneous renal biopsy.
- CT scan of the chest, abdomen, or pelvis: This may be indicated if visceral abscess is suggested.
- Echocardiogram: A transthoracic echocardiogram should be performed if bacterial endocarditis is a possible cause. If findings are inconclusive, a transesophageal echocardiogram is indicated to help rule out valvular vegetations.
Procedures
- Kidney biopsy and other biopsies: These may be helpful depending on the clinical presentation.
Histologic Findings
Depending on the cause, a number of different renal lesions may be seen, as follows:
- Syphilis - Membranous or diffuse proliferative GN
- Hepatitis B - Membranous, membranoproliferative, or mesangial proliferative GN
- Hepatitis C - Membranoproliferative GN (most common), membranous GN (also seen)
- HIV - Focal segmental glomerulosclerosis (classic lesion), membranoproliferative GN or minimal change disease (less common)
- Parvovirus B19 - Focal segmental glomerulosclerosis
- Hantavirus - Mesangial GN
- Schistosomiasis - Mesangial proliferative GN, focal segmental glomerulosclerosis, membranoproliferative GN, or membranous GN
- Leishmaniasis - Mesangial or focal proliferative GN
- Hydatid - Mesangiocapillary GN, membranous GN
- Toxoplasmosis - Mesangioproliferative GN
Treatment
Medical Care
In most cases, the treatment of glomerulonephritis (GN) associated with infection is based on treating the underlying infection. In certain instances, immunosuppressive agents such as corticosteroids may be employed to reduce glomerular inflammation.
- Viral
- Chronic hepatitis B: Treatment is indicated if associated liver dysfunction is present. The usual regimen is interferon alfa-2b at 5 million U/d for 4 months or 10 million U 3 times a week for 4 months. The efficacy of pegylated interferon in regard to hepatitis B related renal disease is unclear at this time. Entecavir and lamivudine have also been used in patients with hepatitis B and GN.
- Chronic hepatitis C: Treatment is with recombinant human interferon alfa at 3 million U 3 times a week for 24 weeks. The pegylated form is long acting and slightly more effective. Preferably, interferon is given along with ribavirin, but this cannot be given in the presence of renal insufficiency. Rituximab has been used to treat hepatitis C related glomerulopathy.
- HIV: Highly active antiretroviral therapy (HAART) is the standard of care for patients with HIV, with or without nephropathy. Treatment is based on findings from viral titers, the history of previous therapy, and, preferably, on the advice of an infectious diseases specialist. There is evidence that HAART therapy may slow the progression of HIV associated nephropathy to end-stage renal disease. Patients should also be started on angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB), as this may slow the progression of disease.
- Other viral agents: Cytomegalovirus, parvovirus, and polyomavirus associated nephropathy are observed in immunocompromised individuals and those who have undergone renal transplantation. Treatment is with specific antiviral agents (ie, ganciclovir for cytomegalovirus and cidofovir for polyomavirus [JC and BK virus]) and temporary withdrawal of immunosuppression therapy.
- Syphilis: Nephropathy is usually observed in secondary syphilis because this phase is associated with high levels of immune complexes. If CNS or ocular involvement is not present, treatment is similar to primary syphilis (ie, single IM dose of benzathine penicillin 2.4 million U). If the patient is allergic to penicillin, use doxycycline (100 mg PO bid) or erythromycin (500 mg PO qid) for 2 weeks.
- Endocarditis: Treatment of shunt infections and visceral abscesses is usually is based on culture sensitivity results.
- Paracytic
- Malaria: Even though falciparum malaria can cause acute tubular necrosis due to acute hemolysis, hypotension chronic-progressive nephropathy is observed with Plasmodium malariae infection. In comparison with falciparum malaria, P malariae infection is a more indolent form of infection, which affects only 25% of erythrocytes and tends to cause chronic progressive immune complex–mediated nephropathy. Treatment with chloroquine is effective for P malariae infection because resistance is uncommon. However, treatment of the infection does not usually slow the progression of nephropathy, and most patients progress to end-stage renal disease in 3-5 years.
- Schistosomiasis: Usually, treatment with praziquantel does not slow the progression of nephropathy. Sometimes, if schistosomiasis is associated with co-infection with Salmonella species, treatment of the Salmonella infection improves the nephropathy.
- Others: Agents used in leishmaniasis treatment include antimony compounds (eg, sodium stibogluconate) and amphotericin B, pentamidine, and paromomycin. Diethylcarbamazepine and ivermectin are used for treating filariasis.
- Fungal: For aspergillosis, treatment is based on the site of infection and usually includes amphotericin.
Surgical Care
If bacterial endocarditis or a shunt infection does not respond to antibiotics, then surgical intervention is indicated.
Consultations
- Consultation with a nephrologist is indicated in patients with GN associated with infection.
- Consultation with an infectious diseases specialist may be appropriate if the infectious etiology is unclear.
Diet
- Salt restriction for is indicated for patients with hypertension.
Activity
- Activity can be performed as tolerated by the patient.
Medication
Antibiotic, antiprotozoal, antiviral, or antifungal agents are used, depending on the cause of infection.
Antibiotics
Therapy must be comprehensive and should cover all likely pathogens in the context of this clinical setting.
Penicillin G benzathine (Bicillin L-A, Permapen)
Interferes with synthesis of cell wall mucopeptides during active multiplication, which results in bactericidal activity.
Dosing
Adult
Syphilis <1 year: 2.4 million U IM once in 2 injection sites
Syphilis >1 year: 2.4 million U IM in 2 injection sites qwk for 3 doses
Pediatric
Syphilis <1 year: 50,000 U/kg IM once; not to exceed 2.4 million U
Syphilis >1 year: 50,000 U/kg IM qwk for 3 doses; not to exceed 2.4 million U
Interactions
Probenecid can increase penicillin effectiveness by decreasing clearance; coadministration with tetracyclines can decrease effectiveness
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in impaired renal function; seizures may occur at high doses
Interferons
Naturally produced proteins with antiviral, antitumor, and immunomodulatory actions. Used for treating hepatitis B and hepatitis C.
Interferon alfa-2b (Intron A)
Indicated for hepatitis B. Protein product manufactured by recombinant DNA technology. Mechanism of antitumor activity not clearly understood; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles.
Dosing
Adult
5 million U/d IM/SC or 10 million U 3 times per wk for 16 wk; reduce dose by 50% if severe reactions occur or temporarily discontinue therapy until symptoms from adverse reactions improve
Pediatric
Not established
Interactions
Potential risk of renal failure when administered concurrently with IL-2; theophylline may increase toxicity by reducing clearance; cimetidine may increase antitumor effects; zidovudine and vinblastine may increase toxicity
Contraindications
Documented hypersensitivity to drug, mouse immunoglobulin (IgG), egg protein, or neomycin; autoimmune hepatitis
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Depression and suicidal ideation may occur; infrequently, severe or fatal GI hemorrhage reported; prior to initiation of therapy, perform tests to quantitate peripheral blood hemoglobin, platelets, granulocytes, hairy cells, and bone marrow hairy cells; monitor periodically (eg, monthly) during treatment to determine response to treatment; if patient does not respond within 6 mo, discontinue treatment; if response occurs, continue treatment until no further improvement observed; not known whether continued treatment after that time is beneficial
Anthelmintics
Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.
Praziquantel (Biltricide)
Increases cell membrane permeability in susceptible worms, resulting in loss of intracellular calcium, massive contractions, and paralysis of musculature. In addition, produces vacuolization and disintegration of schistosome tegument. This is followed by attachment of phagocytes to parasite and death. Tabs should be swallowed whole with some liquid during meals. Keeping tabs in mouth may reveal bitter taste, which can produce nausea or vomiting.
Dosing
Adult
Schistosomiasis: 20 mg/kg PO tid q4-6h
Clonorchiasis and opisthorchiasis: 25 mg/kg PO q4-6h
Hymenolepis: 25 mg/kg PO once
Intestinal infection with Taenia solium, Taenia saginata, Dipylidium caninum, or Diphyllobothrium species: 10-20 mg/kg PO once
Cysticercosis: 50 mg/kg/d PO divided tid for 14 d
Infection with Schistosoma haematobium or Schistosoma mansoni: 40 mg/kg/d PO divided bid once
Infection with Schistosoma japonicum or Schistosoma mekongi: 60 mg/kg/d PO divided tid once
Pediatric
<4 years: Not established
>4 years: Administer as in adults
Interactions
Hydantoins may reduce serum concentrations, possibly leading to treatment failures
Contraindications
Documented hypersensitivity; ocular cysticercosis
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Destruction of parasite within eyes can cause irreparable lesions (ocular cysticercosis should not be treated with praziquantel); caution while driving or performing other tasks requiring alertness on the day of and following treatment; minimal increases in liver enzymes reported; when schistosomiasis or fluke infection associated with cerebral cysticercosis, hospitalize patient for duration of treatment
Diethylcarbamazine citrate (Hetrazan)
For parasitic infections. Synthetic organic compound highly specific for several common parasites. Does not contain toxic metallic elements. Not recommended as DOC because of more severe adverse effects. Recommended if therapy with mebendazole fails or is not available.
Dosing
Adult
3-4 mg/kg/d PO single dose for 4 wk
Pediatric
<2 years: Not recommended
>2 years: Administer as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity; children <2 y
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Start at low dose (25 mg/d) and progressively increase dose to avoid adverse reactions due to parasite lysis
Sodium antimony gluconate (Pentostam)
DOC for the treatment of leishmaniasis in United States. May be administered IV or IM. Intravenous use is preferred because large volumes are required. Available at 100 mg/mL. Dilute each mL in 10 mL of 5% dextrose water and administer over 15 min to prevent thrombophlebitis.
Dosing
Adult
20 mg/kg/d IV (preferred) or IM
Cutaneous disease: Treat for 20 d
Mucocutaneous and visceral disease: Treat for 28 d
Pediatric
<20 kg: Increased dosing may be required to achieve efficacious serum levels; in United States, CDC must approve dose increase
>20 kg: Administer as in adults
Interactions
None reported; patients should avoid taking drugs with similar toxicities and adverse effects, including those that are hepatotoxic or cause QT prolongation
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause myalgias and arthralgias (50%) and GI symptoms (eg, nausea, vomiting, anorexia, abdominal pain); hepatotoxicity and hematologic changes, including decreased WBC, hemoglobin, and platelet counts, can also occur in addition to cardiac dysrhythmias
Chloroquine phosphate (Aralen phosphate)
Inhibits growth by concentrating within acid vesicles of parasite, which increases internal pH of organism. Also inhibits hemoglobin utilization and metabolism of parasite.
Dosing
Adult
600 mg PO on day 1, then 300 mg 6 h later, followed by 300 mg on days 2 and 3
Alternatively, 160-200 mg IM, repeat in 6 h prn; not to exceed 800 mg in first 24 h (change to PO dosing as soon as possible and continue for 3 d until 1.5 g is administered)
Pediatric
10 mg/kg PO on day 1, then 5 mg/kg 6 h later, followed by 5 mg/kg on days 2 and 3
Alternatively, 5 mg/kg IM, repeat in 6 h
Weight-based dosing: 10 mg base/kg PO (not to exceed 600 mg), then 5 mg base/kg PO (not to exceed 300 mg) at 6 h, 24 h, and 48 h to a total of 25 mg/kg
Interactions
Cimetidine may increase serum levels (possibly other 4-aminoquinolones); magnesium trisilicate may decrease absorption of 4-aminoquinolones
Contraindications
Documented hypersensitivity; psoriasis, retinal and visual-field changes attributable to 4-aminoquinolones
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hepatic disease, G-6-PD deficiency, psoriasis, and porphyria; not recommended for long-term use in children; perform periodic ophthalmologic examinations; test for muscle weakness; retinopathy, tinnitus, nerve deafness, skin eruption, headache, anorexia, nausea, vomiting, and diarrhea may occur
Antiviral agents
These agents are nucleoside analogs that inhibit viral replication.
Entecavir (Baraclude)
Guanosine nucleoside analogue with activity against HBV polymerase. Competes with natural substrate deoxyguanosine triphosphate to inhibit HBV polymerase activity (ie, reverse transcriptase). Less effective for lamivudine-refractory HBV infection. Indicated for treatment of chronic hepatitis B infection. Available as tab and oral solution (0.05 mg/mL; 0.5 mg = 10 mL).
Dosing
Adult
Treatment for nucleoside naive: 0.5 mg PO qd 2 h ac or 2 h pc
CrCl 30-49 mL/min: 0.25 mg PO qd or 0.5 mg q48h
CrCl 10-29 mL/min: 0.15 mg PO qd or 0.5 mg q72h
CrCl <10 mL/min: 0.05 mg PO qd or 0.5 mg qwk
Receiving lamivudine or lamivudine resistance: 1 mg PO qd 2 h ac or 2 h pc
CrCl 30-49 mL/min: 0.5 mg PO qd or 1 mg q48h
CrCl 10-29 mL/min: 0.3 mg PO qd or 1 mg q72h
CrCl <10 mL/min: 0.1 mg PO qd or 1 mg qwk
Pediatric
<16 years: Not established
>16 years: Administer as in adults
Interactions
Not a substrate, inhibitor, or inducer of cytochrome P450; coadministration with drugs that reduce renal function (eg, aminoglycosides, cidofovir, cyclosporine) or that compete for active tubular secretion (eg, probenecid, salicylates) may increase serum concentration of either entecavir or coadministered drug
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Reduce dose with renal impairment; if on hemodialysis, administer afterwards; common adverse effects include headache, tiredness, dizziness, and nausea; may elevate liver enzyme levels; may cause lactic acidosis; severe acute exacerbations of hepatitis B may occur in patients who discontinue antihepatitis B therapy
Lamivudine (Epivir-HBV)
Nucleoside analogue approved by the FDA for chronic hepatitis B treatment. Now considered first-line therapy, eclipsing interferon. Inhibits hepatitis B viral DNA polymerase. Use should be considered in patients with ongoing hepatitis B viral replication, elevated aminotransferase activity, and histologic evidence of liver injury. Consider for cases that failed, are unlikely to respond to interferon, or patients who cannot tolerate interferon. Discontinue lamivudine only when repeated assays demonstrated HBeAg loss or seroconversion to HBeAb. Emergence of resistance is the major drawback of nucleoside analogue monotherapy. Proper management of viral breakthrough in patients treated with lamivudine is not yet defined. Continuation of lamivudine appears to be warranted in most cases because resistant strains of HBV seem to be attenuated and are associated with only mild liver injury.
Note that the available dosage forms differ between Epivir and Epivir-HBV (formula specific for hepatitis B virus). Epivir-HVB is available as a 100 mg tab or oral solution 5 mg/mL, whereas Epivir contains 150 mg/tab or 10 mg/mL in oral solution.
Dosing
Adult
100 mg PO qd
Pediatric
<2 years: Not established
2-17 years: 3 mg/kg/d PO qd; not to exceed 100 mg/d
>17 years: Administer as in adults
Interactions
Trimethoprim/sulfamethoxazole increases bioavailability of lamivudine; lamivudine increases concentration of zidovudine when administered concurrently
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Adjust dose in renal impairment; caution in history of pancreatitis
Follow-up
Further Inpatient Care
- Inpatient care depends on the severity of infection, and the need for hospitalization depends on the clinical condition of the patient (eg, the patient may require dialytic support or IV fluids and antibiotics).
Further Outpatient Care
- Oral antibiotics can be continued in an outpatient setting, with frequent monitoring of kidney function. Outpatient dialysis, if necessary, may need to be arranged.
Inpatient & Outpatient Medications
- Oral antibiotics can be continued in an outpatient setting.
Complications
- Deterioration of kidney function may require dialytic support.
Prognosis
- Complete recovery occurs in most patients, even those patients with crescents observed in kidney biopsy tissue.
- The outcome is based on the duration of infection before specific antibacterial or other antiinfective therapy is initiated.
- In schistosomal infections, progression of renal disease is common, even after treatment.
- Nephrotic-range proteinuria may persist for 6 months. A mild increase in protein excretion may be present in 15% of patients at 3 years and in 2-7% of patients at 10 years.
- Microscopic hematuria may persist for 3-6 months after resolution of the syndrome.
Patient Education
- For excellent patient education resources, visit eMedicine's Hepatitis Center, Liver, Gallbladder, and Pancreas Center, and Kidneys and Urinary System Center. Also, see eMedicine's patient education articles Hepatitis B, Hepatitis C, and Blood in the Urine.
Miscellaneous
Medicolegal Pitfalls
- Failure to accurately diagnose
References
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Atta MG, Gallant JE, Rahman MH, et al. Antiretroviral therapy in the treatment of HIV-associated nephropathy. Nephrol Dial Transplant. Oct 2006;21(10):2809-13. [Medline].
Barsoum R. The changing face of schistosomal glomerulopathy. Kidney Int. Dec 2004;66(6):2472-84. [Medline].
Chadban SJ, Atkins RC. Glomerulonephritis. Lancet. May 21-27 2005;365(9473):1797-806. [Medline].
Conlon PJ, Jefferies F, Krigman HR, et al. Predictors of prognosis and risk of acute renal failure in bacterial endocarditis. Clin Nephrol. Feb 1998;49(2):96-101. [Medline].
Haffner D, Schindera F, Aschoff A, et al. The clinical spectrum of shunt nephritis. Nephrol Dial Transplant. Jun 1997;12(6):1143-8. [Medline].
Jefferson JA, Johnson RJ. Treatment of hepatitis C-associated glomerular disease. Semin Nephrol. May 2000;20(3):286-92. [Medline].
Kamar N, Izopet J, Alric L, et al. Hepatitis C virus-related kidney disease: an overview. Clin Nephrol. Mar 2008;69(3):149-60. [Medline].
Lu TC, Ross M. HIV-associated nephropathy: a brief review. Mt Sinai J Med. May 2005;72(3):193-9. [Medline].
Sorger K. Postinfectious glomerulonephritis. Subtypes, clinico-pathological correlations, and follow-up studies. Veroff Pathol. 1986;125:1-105. [Medline].
Tang S, Lai FM, Lui YH, et al. Lamivudine in hepatitis B-associated membranous nephropathy. Kidney Int. Oct 2005;68(4):1750-8. [Medline].
Wyatt CM, Rosenstiel PE, Klotman PE. HIV-associated nephropathy. Contrib Nephrol. 2008;159:151-61. [Medline].
Keywords
glomerular diseases associated with infection, glomerular disease, infection-related glomerulonephritis, GN, postinfectious glomerulonephritis, PIGN, bacterial infection, viral infection, protozoal infection, helminth infection, bacterial endocarditis, shunt nephritis, visceral abscesses, syphilis, hepatitis B, hepatitis C, human immunodeficiency virus, HIV, cytomegalovirus, CMV, parvovirus B19, Hantavirus, malaria, schistosomiasis, leishmaniasis, filariasis, hydatid disease, toxoplasmosis, aspergillosis
Contributor Information and Disclosures
Author
James W Lohr, MD, Fellowship Program Director, Professor, Department of Internal Medicine, Division of Nephrology, State University of New York at Buffalo
James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research
Disclosure: Nothing to disclose.
Coauthor(s)
Quresh T Khairullah, MBBS, Consulting Staff, Department of Medicine, Division of Nephrology, St John's Hospital and Medical Center
Quresh T Khairullah, MBBS is a member of the following medical societies: American College of Physicians, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.
Medical Editor
Frank C Brosius III, MD, Nephrology Program Director, Department of Internal Medicine, Division of Nephrology, Professor of Internal Medicine and Physiology, University of Michigan School of Medicine
Frank C Brosius III, MD is a member of the following medical societies: Alpha Omega Alpha, American Diabetes Association, American Society of Nephrology, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Managing Editor
Ajay K Singh, MB, MRCP, MBA, Associate Professor of Medicine, Director of Dialysis, Department of Medicine, Harvard Medical School; Clinical Chief of Renal Division, Brigham and Women's Hospital
Disclosure: Nothing to disclose.
CME Editor
Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Roche Honoraria Consulting
Chief Editor
Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.
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