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Common Urological Problems

Poststreptococcal Glomerulonephritis

  • - General Urology - Common Urological Problems - Medical Renal Disease
  • Jul 29, 2010
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  • Viewed: 42114
  
Tags: | erythrocyte casts | generalized edema | gross hematuria | hematuria |

A. ESSENTIALS OF DIAGNOSIS

  • History of streptococcal infection
  • Mild generalized edema,  mild hypertension,  retinal hemorrhages
  • Gross hematuria; protein, erythrocyte casts, granular and hyaline casts, white blood cells (leukocytes), and renal epithelial cells in urine
  • Elevated antistreptolysin O titer, hypocomplementemia

B. GENERAL CONSIDERATIONS
Poststreptococcal glomerulonephritis is a disease affecting both kidneys. In most cases recovery from the acute stage is complete, but progressive involvement may destroy renal tissue,  leading to renal insufficiency.  Acute glomerulonephritis is most common in children aged 3-10 years. By far the most common cause is an antecedent infection of the pharynx and tonsils or of the skin with group A betahemolytic streptococci, certain strains of which are nephritogenic.  Nephritis occurs in 10-15%  of children and young adults who have clinically evident infection with a nephritogenic strain. 

In children under age 6,  pyoderma (impetigo) is the most common antecedent; in older children and young adults, pharyngitis is a common antecedent.  Occasionally,  nephritis may follow infection due to other agents, hence the more general term postinfectious glomerulonephritis.

Diagnosis of Medical Renal Disease

Medical Renal Disease

The pathogenesis of the glomerular lesion has been further elucidated by the use of new immunologic techniques (immunofluorescence)  and electron microscopy.  A likely sequel to infection is injury to the mesangial cells in the intercapillary space.  The glomerulus may then become more easily damaged by antigen-antibody complexes developing from the immune response to the infection.

Complement is deposited in association with IgG or alone in a granular pattern on the epithelial side of the basement membrane.

Gross examination of the involved kidney shows only punctate hemorrhages throughout the cortex. Microscopically,  the primary alteration is in the glomeruli,  which show proliferation and swelling of the mesangial and endothelial cells of the capillary tuft. The proliferation of capsular epithelium occurs and around the tuft there are collections of leukocytes,  erythrocytes,  and exudate. 

Edema of the interstitial tissue and cloudy swelling of the tubular epithelium are common. When severe, typical histologic findings in glomerulitis are enlarging crescents that become hyalinized and converted into scar tissue and obstruct the circulation through the glomerulus. Degenerative changes occur in the tubules, with fatty degeneration, necrosis, and ultimately scarring of the nephron.

C. CLINICAL FINDINGS
1. Symptoms and signs- Often the disease is mild, and there may be no reason to suspect renal involvement unless the urine is examined. In severe cases, about 2 weeks after the acute streptococcal infection,  the patient has headache,  malaise,  mild fever,  puffiness around the eyes and face,  flank pain,  and oliguria.  Hematuria is usually noted as “bloody” or, if the urine is acid, as “brown” or “coffee colored.”  There may be moderate tachycardia, dyspnea, and moderate to marked elevation of blood pressure. Tenderness in the costovertebral angle is common.

2. Laboratory findings-
The diagnosis is confirmed by examination of the urine, which may be grossly bloody or coffee colored (acid hematin)  or may show only microscopic hematuria.  In addition,  the urine contains protein (1-3+) and casts. Hyaline and granular casts are commonly found in large numbers, but the classic sign of glomerulitis, occasionally noted, is the erythrocyte cast. The erythrocyte cast is usually of small caliber,  is intensely orange or red, and may show the mosaic pattern of the packed erythrocytes held together by the clot of fibrin and plasma protein.

With the impairment of renal function (decrease in glomerular filtration rate and blood flow)  and with oliguria,  plasma or serum urea nitrogen and creatinine become elevated, the levels varying with the severity of the renal lesion.  A mild normochromic anemia may result from fluid retention and dilution. Infection of the throat with nephritogenic streptococci is frequently followed by increasing antistreptolysin O titers in the serum, whereas high titers are usually not demonstrable following skin infections. Serum complement levels are usually low.

Confirmation of diagnosis is made by examination of the urine, although the history and clinical findings in typical cases leave little doubt. The finding of erythrocytes in a cast is proof that erythrocytes were present in the renal tubules and did not arise from elsewhere in the genitourinary tract.

3. Treatment-
There is no specific treatment. Eradication of infection, prevention of overhydration and hypertension,  and prompt treatment of complications such as hypertensive encephalopathy and heart failure require careful management.

4. Prognosis-
Most patients with the acute disease recover completely; 5-20% show progressive renal damage.

This damage may be evident only years after the immune injury. If oliguria, heart failure, or hypertensive encephalopathy is severe, death may occur during the acute attack.

Even with severe acute disease,  however,  recovery is the rule, particularly in children.

***
Flavio G. Vincenti, MD, & William J.C. Amend, Jr., MD

***
REFERENCES

  1. Adler S: Diabetic nephropathy: Linking histology, cell biology, and genetics. Kidney Int 2004;66:2095.
  2. Alric L et al: Influence of antiviral therapy in hepatitis C virus-associated cryoglobulinemic MPGN. Am J Kidney Dis 2004;43:617.
  3. Appel GB et al: Membranoproliferative glomerulonephritis Type II (dense deposit disease): An update. J Amer Soc Neph 2005;16: 1392.
  4. Barratt J, Feehally J: IgA nephropathy. J Amer Soc Neph 2005;16: 2088.
  5. Braden GL et al: Tubulointerstitial diseases. Am J Kidney Dis 2005; 46:560.
  6. Buhaescu I et al: Systemic vasculitis: Still a challenging disease. Am J Kidney Dis 2005;46:173.
  7. Chesney R: The changing face of childhood nephrotic syndrome. Kidney Int 2004;66:1294.
  8. Flanc RS et al: Treatment of diffuse proliferative lupus nephritis: A meta-analysis of randomized controlled trials. Am J Kidney Dis 2004;43:197.
  9. Couser WG (guest editor): Frontiers in nephrology: Membranous nephropathy. J Amer Soc Neph 2005;16:1184.
  10. Ginzler EM et al: Mycophenolate mofetil or intravenous cyclophosphamide for lupus nephritis. N Engl J Med 2005;353:2219.
  11. Grantham JJ: Advancement in the understanding of polycystic kidney disease: A system approach. Kidney Int 2003;64: 1154.
  12. Heering P et al: Cyclosporine A and chlorambucil in the treatment of idiopathic focal segmental glomerulosclerosis. Am J Kidney Dis 2004;43:10.
  13. Hruska KA: Treatment of chronic tubulointerstitial disease: A new concept. Kidney Int 2002;61:1911.
  14. Imaging the Kidney-Radiologic Imaging 2006. (Excerpts) Nephron Clin Pract 2006;103:c19.
  15. Izzedine H et al: Oculorenal manifestations in systemic autoimmune diseases. Am J Kidney Dis 2004;43:209.
  16. Javaid B, Quigg RJ: Treatment of glomerulonephritis: Will we ever have options other than steroids and cytotoxics? Kidney Int 2005;67:1692.
  17. Nair R, Walker PD: Is IgA nephropathy the commonest primary glomerulopathy among young adults in the USA? Kidney Int 2006;69:1455.
  18. Noris M, Remuzzi G: Hemolytic uremic syndrome. J Amer Soc Neph 2005;16:1035.
  19. Perna A et al: Immunosuppressive treatment for idiopathic membranous nephropathy: A systematic review. Am J Kidney Disease 2004;44:385.
  20. Rosner MH, Bolton WK: Renal function testing. Am J Kidney Dis 2006;47:174.
  21. Rossert J: Drug-induced acute interstitial nephritis. Kidney Int 2001; 60:804.
  22. Tenenhouse HS, Murer H: Disorders of renal tubular phosphate transport. J Am Soc Neph 2003;14:240.
  23. Troyanov S et al: Renal pathology in idiopathic membranous nephropathy: A new perspective. Kidney Int 2006;69:1641.
  24. Wilmer WA et al: Management of glomerular proteinuria: A commentary. J Amer Soc Neph 2003;14:3217.

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