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Diffuse Proliferative Glomerulonephritis Clinical Presentation

  • Author: Moro O Salifu, MD, MPH, FACP; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Apr 28, 2015
 

History

Focus the history on the causes of DPGN and the associated symptoms. While a minority of patients may be asymptomatic (ie, < 15%) and are diagnosed during routine laboratory examination, most patients manifest signs of the primary disease as well as those relating to renal injury.

  • Suspect DPGN in patients with SLE, infectious disease processes, a recent streptococcal throat infection, or in patients with sinopulmonary disease who have recent onset of the following:
    • Hypertension
    • Microscopic or gross hematuria
    • Nonnephrotic or nephrotic range proteinuria or an increase in proteinuria from baseline
    • Serum creatinine of more than 0.4 mg/dL from the reference range or the baseline
    • Oligoanuria and symptoms of uremia in severe cases of RPGN with crescent formation
  • Also suspect DPGN in a patient with other systemic diseases who has recent onset of the same findings listed above.
  • Nonspecific symptoms, including nausea, vomiting, fatigue, or weight loss may indicate uremia or symptoms of the primary disease process.
  • A history of rash; photosensitivity; oral ulcers; arthralgias; arthritis; serositis; or a renal, neurologic, hematologic, or immunologic disorder suggests SLE as the primary disease.
  • A history of cough, dyspnea, hemoptysis, and renal disease suggests Goodpasture syndrome, but other pulmonary-renal syndromes must be ruled out, including SLE pneumonitis, Wegener granulomatosis, cryoglobulinemia, renal vein thrombosis with pulmonary embolism, legionella infection, and congestive heart failure.
  • Patients with Wegener granulomatosis present with sinopulmonary disease (ie, paranasal sinus pain and drainage with purulent or bloody nasal discharge and occasional nasal mucosal ulceration/perforation, leading to saddle nose deformity), serous otitis media (ie, blockage of the eustachian tube), cough, dyspnea, and hemoptysis.
  • Patients with IgA nephropathy (ie, Berger disease) may present with the classic findings of flank pain and gross hematuria following upper respiratory infections. Others may simply have indolent microhematuria found incidentally. Much less commonly, patients present with acute glomerulonephritis, renal failure, and nephrotic syndrome.
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Physical

See the list below:

  • If azotemia is present, exclude prerenal and postrenal causes.
  • Nonspecific findings that suggest DPGN
    • Hypertension
    • Fever, present in infectious and noninfectious glomerulonephritis
  • Findings pertaining to SLE include the often acute onset of conjunctivitis, episcleritis, photosensitivity, oral ulcers, malar rash (eg, erythema of the nose and malar eminences in a butterfly distribution), discoid lupus, pleural or pericardial friction rub, psychosis, seizures, nonerosive arthritis, or arthralgia
  • Findings relating to pauci-immune disease (eg, anti-GBM disease, Wegener granulomatosis) and Goodpasture syndrome
    • Sinusitis, otitis, saddle nose deformity, hemoptysis
    • Lung consolidation, which suggests pulmonary hemorrhage
  • Findings relating to IgA nephropathy (usually postinfectious) and other infectious glomerulonephritis
    • Pharyngitis, gastroenteritis
    • Impetigo, which is the most common cause of poststreptococcal glomerulonephritis worldwide
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Causes

See the list below:

  • Immunoglobulin A (IgA) nephropathy and SLE are the most common causes. Other etiologies are less frequent but are more likely to lead to RPGN.
  • Systemic diseases
    • Lupus nephritis class IV, IgA nephropathy
    • Goodpasture syndrome, Wegener granulomatosis, microscopic polyangiitis, Henoch-Schönlein purpura
    • Cryoglobulinemia, vasculitis
  • Infectious causes
    • Poststreptococcal glomerulonephritis, which occurs 2-4 weeks after streptococcal sore throat or skin infection
    • Infective endocarditis, hepatitis B, hepatitis C
  • Histologic transformation
    • In patients with class IV lupus nephritis, histologic transformation from one class to another is recorded in up to 40% of repeat biopsies.
    • The most likely transformation is from class II or III to class IV. Any other class may be superimposed on class V.
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Contributor Information and Disclosures
Author

Moro O Salifu, MD, MPH, FACP Associate Professor, Department of Internal Medicine, Chief, Division of Nephrology, Director of Nephrology Fellowship Program and Transplant Nephrology, State University of New York Downstate Medical Center

Moro O Salifu, MD, MPH, FACP is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Society of Transplantation, American Society of Diagnostic and Interventional Nephrology, American Medical Association, American Society for Artificial Internal Organs, American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

Coauthor(s)

Barbara G Delano, MD, MPH, FACP Professor and Chair, Department of Community Health Sciences, School of Public Health, State University of New York Downstate

Barbara G Delano, MD, MPH, FACP is a member of the following medical societies: American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ajay K Singh, MB, MRCP, MBA Associate Professor of Medicine, Harvard Medical School; Director of Dialysis, Renal Division, Brigham and Women's Hospital; Director, Brigham/Falkner Dialysis Unit, Faulkner Hospital

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, 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, International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

James H Sondheimer, MD, FACP, FASN Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director of Hemodialysis, Harper University Hospital at Detroit Medical Center; Medical Director, DaVita Greenview Dialysis (Southfield)

James H Sondheimer, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology

Disclosure: Receive dialysis unit medical director fee (as independ ent contractor) for: DaVita .

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Light microscopy (trichrome stain) shows globally increased cellularity, numerous polymorphonuclear cells, cellular crescent (at left of photomicrograph) and fibrinoid necrosis (brick red staining at right of photomicrograph). These findings are characteristic of diffuse proliferative glomerulonephritis.
Diffuse proliferative glomerulonephritis (DPGN). Immunofluorescent microscopy shows (except for anti–glomerular basement membrane [GBM] disease) a granular deposition of immunoglobulins, complement, and fibrin along the GBM, tubular basement membranes, and peritubular capillaries (image 2a). Linear deposition occurs in the GBM in anti-GBM disease (image 2b).
Diffuse proliferative glomerulonephritis (DPGN). Using electron microscopy, electron-dense deposits are visible in the mesangial, subendothelial, intramembranous, and subepithelial locations.
 
 
 
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