Renal and Systemic Hemodynamics in Falciparum Malaria

Abstract

Renal and systemic hemodynamics, plasma arginine vasopressin, plasma renin activity, plasma norepinephrine, blood volume and water loading test were studied in 10 patients with falciparum malaria without renal failure. Six patients responded to water load normally, while 4 patients had a decreased response to water load. The patients with a normal water load response had normal renal and systemic hemodynamics and a normal hormonal profile. The patients with a decreased response to water load had hyponatremia, hypervolemia, high cardiac index, low systemic vascular resistance, high plasma arginine vasopressin, high plasma renin activity, high plasma norepinephrine, low creatinine and p·aminohippurate clearances, low urine sodium and high urine osmolality. They had a lower mean arterial pressure during the acute phase of the disease than during the recovery phase. The findings suggest that a decreased response to water load is due to peripheral vasodilatation which results in a decreased effective blood volume leading to the release of vasopressin and norepinephrine, increased renin activity and decreased renal hemodynamics.

Is the development of falciparum malaria in the human host limited by the availability of uninfected erythrocytes?

“…The first generation of post capillary venules range in size from 10 μm to 30 μm and the second generation from 40 μm to 200 μm, whereas the diameter of the spherical PRBC is not larger than 4.4 μm. There is, therefore, plenty of room for circulation to continue, especially with vasodilatation, for which there is some evidence of occurrence in malaria infections [23-25]. PRBC are more rigid and less deformable than uninfected RBC (although these are also less deformable than normal RBC) [26,27] and thus increase blood viscosity [28-30].…”

“…Histology, however, indicates that even in severe malaria not all venules are obstructed. Vasodilatation, which has been observed by some investigators in malaria patients [23,43], is known not to affect venules directly, but feeding arteries and arterioles. Flow in capillaries in the healthy host is typically intermittent and not all capillaries necessarily allow blood flow all the time.…”

“…Investigations have shown that in malaria patients' blood flow is restricted through the kidney [23,45,46], the liver [47,48], the brain [49,50], the placenta [51] and that in Plasmodium berghei infection there is a general failure of capillary flow and disruption of venous outflow tracts by aggregates of infected and uninfected cells [52]. Another report could not find evidence for hypoperfusion in cerebral malaria [53].…”

Leptospiral Acute Renal Failure: Effects of Dopamine and Furosemide

“…[8,9] This is similar to the findings in malaria. [10] At the clinical level, there may be subclinical hypotension or clinical hypotension when the disease is severe. [11] A decreased response to fluid load has been observed.…”

A Retrospective Analysis of the Haemodynamic and Metabolic Effects of Fluid Resuscitation in Vietnamese Adults with Severe Falciparum Malaria

“…Small series have confirmed that some adult patients with severe malaria are hypovolaemic, or at least have a reduced effective circulating volume [7], [8]. This hypovolaemia has the potential to exacerbate renal failure and lactic acidosis, two of the most significant contributors to mortality in severe malaria [9].…”