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Common Urological Problems

Clinical Findings in Nephrosis

  • - General Urology - Common Urological Problems - Medical Renal Disease
  • Jul 29, 2010
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Tags: | amyloid disease | diabetic nephropathy | edema | lupus erythematosus |

A. SYMPTOMS AND SIGNS
Edema may appear insidiously and increase slowly or can appear suddenly and accumulate rapidly. Symptoms other than those related to the mechanical effects of edema are not remarkable.

On physical examination, massive peripheral edema is apparent.  Signs of hydrothorax and ascites are common.

Pallor is often accentuated by the edema, and striae commonly appear.

B. LABORATORY FINDINGS
The urine contains large amounts of protein, 4-10 g/24 h or more.  There is a good correlation between the urine protein to creatinine ratio (from a “spot” AM urine) and the 24-hour. proteinuria. For example, a ratio in excess of 3:1 in the spot urine usually correlates to a 24-hour proteinuria of 3 g. The sediment contains casts, including the characteristic fatty and waxy varieties;  renal tubular cells, some of which contain fatty droplets (oval fat bodies); and variable numbers of erythrocytes.  A mild normochromic anemia is common,  but anemia may be more severe if renal damage is great. Nitrogen retention varies with the severity of impairment of renal function. 

Diagnosis of Medical Renal Disease

Medical Renal Disease

The plasma is often lipemic, and the blood cholesterol is usually greatly elevated. Plasma protein is greatly reduced. The albumin fraction may fall to less than 2 g/dL. Serum complement is usually low in active disease. The serum electrolyte concentrations are often normal, although the serum sodium may be slightly low; total serum calcium may be low, in keeping with the degree of hypoalbuminemia and decrease in the protein-bound calcium moiety. During edema-forming periods, urinary sodium excretion is very low and urinary aldosterone excretion is elevated. If renal insufficiency (see preceding discussion) is present, the blood and urine findings are usually altered accordingly.

Renal biopsy is often essential to establish the diagnosis between the various conditions and to indicate prognosis.

C. DIFFERENTIAL DIAGNOSIS
The nephrotic syndrome (nephrosis)  may be associated with a variety of primary renal diseases or may be secondary to a systemic process:  collagen-vascular diseases (eg, disseminated lupus erythematosus,  polyarteritis),  diabetic nephropathy,  amyloid disease,  thrombosis of the renal vein,  myxedema,  multiple myeloma,  malaria,  syphilis, reaction to toxins or heavy metals, reactions to drugs, and constrictive pericarditis.

D. TREATMENT
An adequate diet with restricted sodium intake (0.5-1 g/d) and prompt treatment of intercurrent infection are the basis of therapy.  Diuretics may be given but are often only partially effective.  Salt-free albumin and other oncotic agents are of little help, and their effects are transient.  The corticosteroids have been shown to be of value in treating nephrotic syndrome when the underlying disease is of minimal change-focal segmental glomerulosclerosis,  systemic lupus erythematosus,  or proliferative and crescentic glomerulonephritis.

Steroids are often less effective in the treatment of membranous disease and membranoproliferative lesions of the glomerulus.

Alkylating agents, azathioprine, mycophenolate mofetil, cyclosporine,  and tacrolimus,  have been used in the treatment of nephrotic syndrome.  Encouraging early results have been reported in children and adults with proliferative or membranous lesions and with systemic lupus erythematosus. It is not known what percentage of patients can be expected to benefit from these drugs.

Both corticosteroids and cytotoxic agents are commonly associated with serious side effects. At present, this form of therapy should be employed only in patients in whom the disease has proved refractory to well-established treatment regimens.

Reduction in proteinuria and improvement in nephrotic edema have been reported using low-protein diets and angiotensin-converting enzyme (ACE)  inhibitors or angiotensin receptor blockers (ARBs). Most recently, studies have shown some improvements with lipid-lowering drugs.

E. PROGNOSIS
The course and prognosis depend on the basic disease responsible for nephrotic syndrome. In most children with nephrosis (usually secondary to minimal change nephropathy),  the disease appears to run a rather benign course when properly treated and to leave insignificant sequelae.

Of the remaining children, most go inexorably into renal insufficiency. Adults with nephrosis fare less well. Hypertension, heavy proteinuria, and renal dysfunction are poor prognosticators.


***
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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