Severe nephrotic syndrome without oedema in a patient with HIV associated nephropathy

Hassane Izzedine, Maud François and Gilbert Deray

Department of Nephrology, Pitié Salpétrière Hospital, Paris, France

Sir,

Human immunodeficiency virus associated nephropathy (HIVAN) is a clinical entity characterized by a nephrotic syndrome and rapid progression to renal failure. The severity of proteinuria often contrasts with the conspicuous absence of peripheral oedema, which is usually explained by high plasma globulin level and/or hypovolaemia. We report on a patient with severe nephrotic proteinuria without oedema who had normal plasma globulin level and envolaemia.

In this 32-year-old woman, HIVAN was first diagnosed in October 1998. A kidney biopsy had been performed because of renal failure and proteinuria. She was then treated with lamivudine, stavudine and ritonavir. She was hospitalized in December 1998 for rapid progression of renal failure and severe nephrotic syndrome (albuminaemia 6 g/l, proteinuria 35 g/24 h). She had stopped her antiretroviral treatment 3 weeks previously because of acute pancreatitis.

Serum proteins, blood urea nitrogen (BUN) and creatinine measurements were obtained at the Pitié Salpétrière Paris Hospital Laboratory (Table 1Go). We calculated total oncotic pressure using the formula of Nitta et al. [1]:


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Table 1. Comparison of HIV patients without oedema
 
COPpl:

where COPpl is the plasma protein colloid osmotic pressure (mmHg) at pH 7.4, 37°C, and electrolytes concentration of 0.15 mol/l, {alpha} and ß represent albumin and globulin fraction, respectively and c represents protein concentration (g/100 ml).

In the literature more than 30% of patients with HIVAN presented without peripheral oedema even when albumin was reduced to about 22 g/l [2]. It has been suggested that HIV patients may maintain higher oncotic pressure secondary to increased globulins, resulting in a lower incidence of oedema when compared with other patients in similar situations [3]. Indeed Guardia et al. have shown that globulins play an important role in maintaining oncotic pressure in cases with low albumin [3]. By contrast, Perinbasekar [4] has suggested that haemodynamic factors such as hypovolaemia may play a role in the frequent absence of oedema in patients with HIV infection and renal failure.

In our case, we failed to observe oedema despite a dramatic decrease in serum albumin, a normal globulin level, and aggressive plasma volume expansion to increase central venous pressure up to 10 cmHg.

In summary, the reason for the absence of peripheral oedema in HIVAN remains unclear. Our case argues against the hypotheses that have been advanced to explain this paradox, i.e. high globulin concentrations and hypovolaemia. Other mechanisms are probably involved in this clinical curiosity.

References

  1. Nitta S, Ohnuki T, Ohkuda K, Nadaka T, Staub NC. The corrected protein equation to estimate plasma colloid osmotic pressure and its development on a monogram. Tohoku J Exp Med 1981; 135: 43–49[ISI][Medline]
  2. Bourgoignie JJ, Meneses R, Pardo V. The nephropathy related to acquired immunodeficiency syndrome. Adv Nephrol 1988; 17: 113–126
  3. Guardia JA, Ortiz-Butcher C, Bourgoignie JJ. Oncotic pressure and oedema formation in hypoalbuminemic HIV infected patients with proteinuria. Am J Kidney Dis 1997; 30: 822–828[ISI][Medline]
  4. Perinbasekar S, Brod-Miller C, Mattana J. Absence of edema in HIV-infected patients with end-stage renal disease. Acquired Immune Deficiency Syndromes Hum Retrovirol 1996; 13: 368–373




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