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J Am Soc Nephrol 11: 2147–2154, 2000
Malarial Acute Renal Failure
RASHAD S. BARSOUM
Department of Internal Medicine, Nephrology Unit, Cairo University, Cairo, Egypt.
Malaria is an Italian word composed of “mala ” and “aria,” derived from malus (bad), and aeris (air). It was first used to describe a fever (miasma), which was wrongly attributed to exposure to poisonous air rising from marshes. Although the disease had been described in the Hippocratic Collection (460 to 377 BC) and its relation to mosquitoes suggested in the 5th century AD, by the Indian physician Susruta, it was only in 1880 that Charles Laveran, a French physician working in Algeria, discovered the true causative agent as being a sporozoan of the genus Plasmodium. More than a century later, we got to map the malaria genome, identifying a huge number of genes located on 14 chromosomes. Malaria is acquired through the sting of an infected Anopheles mosquito, which injects the sporozoites into the host’s dermis. These are carried with the blood stream to the liver, where they mature in the hepatocytes (extra-erythrocytic cycle) to tissue schizonts that release their merozoites into the hepatic sinusoids. The latter invade the red cells, starting the erythrocytic cycle, which comprises ring forms, trophozoites, and, subsequently, schizonts that contain a new generation of merozoites. The parasitized cells are induced by plasmodial DNA to develop a microtubular system that conveys nutrients to the parasite. They eventually rupture and release the merozoites, which repeat the same cycle. A few merozoites are sexually differentiated into male and female gametocytes, which are essential for the completion of the sexual cycle in the vector.
known for many centuries. Celebrities known to have contracted the disease while traveling to Africa or Asia include the Italian poet Guido Cavalcanti in 1300, the British explorer Sir Richard Burton in 1858, and the American president John F. Kennedy while serving in the Pacific during World War II. Malaria in nonimmune Caucasians is notoriously severe, with cerebral and renal complications often supervening with a fatal outcome. Infected mosquitoes can also travel with passengers or cargo and have been reported to transmit the disease to visitors of major European airports (“airport malaria”). They could even establish endemic foci in the West as reported from Belgium and the United States.
Several species affect humans, leading to different patterns of the disease. The most important are Plasmodium falciparum, which causes falciparum malaria, P. malariae, which causes Quartan malaria, and P. vivax and P. ovale, which cause tertian malaria. Genetic interspecies differences explain the variance in the clinical syndromes caused by these sporozoans. These include the rate of multiplication, expression of different antigenic and ligand proteins on the host’s parasitized cells, influence of host factors on the parasite’s antigenic variability, and others. A striking expression of this divergence is the ability of different strains to invade human red cells of different ages. Thus, P. vivax and P. ovale infect only young red cells, whereas P. malariae infects only aging cells. P. falciparum invades erythrocytes at any age, which explains the heavy parasitemia associated with this species. In contrast, erythrocytes with hemoglobin S typically are resistant to this species. Parasitized erythrocytes initiate the three principal pathogenetic features in plasmodium infections: hemodynamic, immunologic, and metabolic perturbations. The complex malarial syndrome represents the ultimate interaction among these lines (Figure 1).
Malaria is widely spread throughout the world and affects close to 400 million people, most of whom live in Africa, India, Southeast Asia, and Latin America. With the increasing immigration of natives from those regions to Europe and North America, “imported malaria” imposed itself on the list of differential diagnosis of many medical conditions in the West as recurrent fever, jaundice, hemolytic anemia, acute renal failure (ARF), systemic inflammatory response (SIR) syndrome, and posttransplantation pyrexia (1). An increasing number of Caucasians acquire the disease through traveling or living in endemic areas. This risk has been
Parasitized red cells are sticky. They tend to adhere to adjacent healthy erythrocytes (2), blood platelets (3), and the capillary endothelium (4). This results in the formation of intravascular rosettes and clumps, which can impede the microcirculation. Although this feature is observed with all plasmodial infections, its major clinical impact is in falciparum malaria, where it has been long associated with serious sequelae, particularly in the nervous system (5).
Correspondence to Professor Rashad Barsoum, The Cairo Kidney Center, P.O. Box 91 Bab-El-Louk, Cairo, 11513, Egypt. Phone: ϩϩ20-2-5761673; Fax: ϩϩ20-2-5769749; E-mail: firstname.lastname@example.org 1046-6673/1111-2147 Journal of the American Society of Nephrology Copyright © 2000 by the American Society of Nephrology
Other adhesive protein families have been identified in the erythrocyte knobs. the ring-infected erythrocyte surface antigen (16). but their relative pathogenetic significance seems to be less prominent than that of the PfEMP-1. which includes several members identified by sequential numbers. it is the novel polypeptide expression on the parasitized red cells that constitutes the major part of the antigen load. 70-kD and 78-kD heat shock proteins (18). Most of these are also variable proteins of importance in the host–parasite relationship. Although some are constitutively expressed. and endothelin. glycosylphosphatidylinositol moieties covalently linked to the surface antigens of falciparum malarial parasites seem to act like endotoxin that interacts with upregulated monocyte CD14 receptors (19). the Pf332 antigen seems to interact with a . as shown by the effect of splenectomy in experimental models (8). and chodroitin4-sulfate. In addition to the adhesive proteins described earlier. Although all of these antigens are able to activate the peripheral blood mononuclear cells. There are many platelet and endothelial receptors. This “cross talk” between the parasite and the host keeps the balance. The main red cell receptors for PfEMP-1 are the CR1 and glycosaminoglycans (12). other antigenic proteins have been identified on parasitized red cells. but there is no doubt that other local mediators are involved in the ultimate response of the peripheral capillaries to the complex scenario of falciparum malarial infection (14). monocytes.2148 Journal of the American Society of Nephrology J Am Soc Nephrol 11: 2147–2154. These include “var” gene products other than the PfEMP-1 (15). 2000 Figure 1. rosettins (11). and others. Principal pathogenetic pathways in severe falciparum malaria. Immune Perturbation Antigenic proteins are expressed on the cell membranes of both the parasite and the parasitized host cells. as CD36. rifins (10). thereby provoking a Th1 proinflammatory response. The associated endothelial activation leads to the release of several vasoactive cytokines. P-selectin. This is attributed to switching between alleles in the “major var gene” in successive merozoite generations. being structurally and antigenically different in consecutive generations of parasitized red cells. ICAM-1. there is evidence that they provoke a differential immune response. A striking feature of this protein is variability. Conversely. The adhesive ligands on parasitized red cell membranes have long been identified as “knobs” composed of abnormal proteins encoded by the parasite’s genome. including the histidine-rich proteins (9). including E-selectin. Switching is largely a spontaneous process (7) but is also influenced by host factors. which permits both to survive. catecholamines. The major family of adhesive proteins is called plasmodium falciparum erythrocyte membrane proteins (PfEMP) (6). For example. Pf332 (17). and hepatocytes. thrombomodulin. PfEMP-1 seems to be the major determinant of erythrocyte adhesiveness and subsequent malarial morbidity. many are induced by the host’s immune response as a part of widespread endothelial activation. The hemodynamic element in the pathogenesis of malaria is not limited to capillary lumen obstruction by sticky cell aggregates. owing to the intracellular residence of the sporozoan during most of its life cycle in man. and VCAM-1 (13). and others. PECAM-1/CD31. Specifically reported are thromboxane. However.
with IL-2–induced switching to IgG2 synthesis. Together with IL-10. clumping. . favoring IgE and IgG4 synthesis (24). Most notorious in falciparum malaria is the inhibition of the erythrocyte magnesium-activated ATPase (28). Th2 activation has an immune modulatory function and is associated with immunity to reinfection. However. including parasite-derived rosettins (11). It is not clear whether the same or other factors or the abnormal cytokine profile that supervenes in malaria is responsible for the hepatocyte membrane abnormality that leads to cholestatic jaundice in the majority of cases. However. 2000 Malarial Acute Renal Failure 2149 different monocyte receptor that favors Th2 proliferation (17). As mentioned earlier. Many factors have been incriminated in this phenomenon. Because thiamine pyrophosphate is an essential coenzyme for several metabolic key reactions. its depletion may be an additional factor in depressing the host’s aerobic glycolysis. IL-4 downregulates the monocytes and inhibits the release of IL-8. Tissue Hypoxia. Plasmodia consume large quantities of glucose for their own energy requirements. This may be responsible for some of the immunemediated phenomena that cannot be explained by the paucity of circulating immune complexes in this infection. Ig-. They seem to have a mandatory role in the regulation of the early immune response and the elimination of chronic infection. their exact role in this respect is not yet understood. and (4) side effects of treatment. Even nonparasitized red cells suffer membrane changes that lead to rosette formation. particularly the neurologic. falciparum and P. leading to internal dilution hyponatremia. almost invariable in malaria. and other plasma protein abnormalities. The hallmark of proinflammatory monocyte activation is the release of tumor necrosis factor-␣ (TNF-␣). Antibodies to triosephosphate isomerase (23) have been associated with prolonged complement-dependent hemolytic anemia after acute malaria. In addition. antiphospholipid (21). none of the clinical manifestations of severe malaria. depressed mitochondrial respiration (31). In addition to the de novo synthesis of antigenic and adhesive polypeptides encoded by the parasite’s DNA. Anticardiolipin. increased anaerobic glycolysis (Pasteur effect). The same question applies to leaky muscle membranes associated with malarial rhabdomyolysis (29). It also activates the intrinsic coagulation cascade. Inducible nitric oxide generation and abnormal lipid peroxidation are documented consequences of the increased oxidative stress in falciparum malaria (32). and endothelial adhesion of parasitized red cells. A recent study also showed an increase of the serum transketolase activity in patients with falciparum malaria. This indicates thiamine depletion. The release of IL-4 induces B-lymphocyte proliferation. could be statistically correlated to measurable biochemical parameters of thiamine deficiency. P. which participates in the pathogenesis of thrombotic complications (14). Kinetic studies are awaited to confirm this hypothetical conflict between the energy needs of the host and the parasite. which is associated with immunity to reinfection.J Am Soc Nephrol 11: 2147–2154. This impairs the sodium pump in a “sick-cell syndrome” fashion. and lactic acid accumulation. Malarial antigen-IgE antibody complexes are identified by CD23 monocyte receptors. Of equal significance is the release of IL-6. which has a pivotal role in the pathogenesis of acute malarial morbidity (14). Th1 activation also leads to B-lymphocyte proliferation. Cell Membrane Abnormalities. falciparum directly activates C3 through the alternative pathway. leading to increased TNF-␣ generation through a nitric oxide–transduction mechanism. which seems to be crucial in cerebral malaria (26). Secondary calcium influx alters the calmodulin-dependent erythrocyte kinetics. Quinine therapy may lead to further lowering of the blood sugar level owing to the stimulatory effect of the drug on the pancreatic ␤ cells (29). Shortened red-cell survival is. rosette formation is an important contributor to the disturbed peripheral blood rheology in malaria. therefore. This often leads to autoantibody formation that is usually associated with P. often leading to clinically overt hypoglycemia. the release of local cytokines. Metabolic Disturbance The metabolic abnormalities associated with plasmodial infection are the consequence of (1) perturbation of the host’s red cell membranes. This is particularly manifest in cerebral malaria. changes in the constitutive parasitized cell membrane structure may lead to important functional abnormalities. reduces hemoglobin– cell wall interaction. This further augments the peripheral hemodynamic derangement and increases the erythrocyte mechanical fragility. and increased generation of reactive oxygen molecules. The interaction of TNF-␣ and IL-5 leads to eosinophil activation. This seems to overwhelm the host’s compensatory mechanisms. The observed increase in neopterin serum levels in malignant malaria is the consequence of this augmented release of interferon-␥. The metabolic consequences of tissue hypoxia and potential impairment of glucose availability include increased lactic acid production with increased lactate/pyruvate ratio (29). vivax infections. The latter secrete interferon-␥. and antineutrophil cytoplasmic (22) antibodies have been suggested to have a role in the pathogenesis of microvascular complications. which is the main proliferative signal for Th1 cells. Peripheral ␥-␦ T lymphocytes are strongly upregulated in malaria (27). where IgE antibody levels are considerably elevated (25). Th2 lymphocytes have been recently shown to behave as proinflammatory cells. The disturbed peripheral blood rheology induced by rosetting. which amplifies the monocyte response by a positive feed back mechanism (20). and curtails red cell deformability. (3) repercussions of the described hemodynamic and immunologic disturbances. and the immune-mediated systemic inflammatory response all contribute to peripheral pooling and impeded tissue oxygenation. which is attributed to the increased demand for the parasite’s glycolytic pathway (30). (2) the parasite’s consumption of nutrients and cofactors. Parasite’s Energy Consumption.
C3. The disease affects children. The contribution of malaria to the overall hospital admissions for ARF varies from 2 to 39% (29. The spleen may be enlarged. Renal Involvement in Malaria There are two major renal syndromes associated with Malaria (1): (1) a chronic and progressive glomerulopathy that mainly affects African children. with subendothelial immune complex deposits containing IgG.5 3 1 Average of reported figures. Acute Malarial Nephropathy ARF complicates falciparum malaria in fewer than 1 to 4. malariae is the established cause of chronic malarial nephropathy (29). True malarial hepatitis also occurs in approximately 20% of cases. occurring in more than 75% of cases (34). Most cases are oliguric.” with an unconjugated component resulting from the excessive hemolysis and a conjugated element resulting from cholestasis.2 6 6 6 4. DNA probes have been introduced but are not yet widely applicable. falciparum is the causative species in the overwhelming majority of cases. and other factors. It typically is hemolytic. The characteristic histopathologic lesion is mesangio- Table 1. followed by rapid increase in temperature that lasts for a few hours before resolving by crisis associated with excessive sweating. . more often in ex-patriots and during the first infection episode in natives.2 21 20 18. usually 4 to 8 yr old. Peripheral blood pooling as a result of dramatic reduction of the peripheral vascular resistance occurs in two thirds of cases. Anemia occurs in at least 70% of patients and is reported as being severe in 40%. vivax occasionally is incriminated.33) according to the local prevalence of the disease. capillary glomerulonephritis. India. vivax. particularly with relapsing disease. which is hallmarked by elevated serum transaminases. A recent report suggests the hemophagocytic syndrome as the cause of severe anemia in a Japanese patient who acquired falciparum infection during a visit to the tropics (35). Figure 2. The disease proceeds to renal failure even after successful eradication of the infection. and muscle and joint aches are usually encountered. pigment deposition. then it occurs less frequently with a tendency to periodicity. foci of steatosis. half of which develop an overt bleeding tendency.2150 Journal of the American Society of Nephrology J Am Soc Nephrol 11: 2147–2154. may be repeated several times during the first day or two of clinical illness. Incidence of complications in faclicparum malaria in six different seriesa Complication Incidence (%) Hemolysis Jaundice Cerebral Thrombocytopenia Pancytopenia Diarrhea Systemic inflammatory response Acute respiratory distressa Acute renal failurea Death a 46. and malarial antigens. particularly alanine aminotransferase. which corresponds to the completion of one of the parasite’s erythrocytic cycles and subsequent lysis of infected red cells. Chronic Malarial Nephropathy P. P. yet it is much more frequent in nonimmune Europeans. hypercatabolic. In the majority of cases. this is part of a disseminated intravascular coagulation initiated by the gross rheologic abnormality in severe malaria (29). It typically is “biphasic. and sub-Saharan Africa (Figure 2). Thrombocytopenia occurs in 70% of cases. Serology is of limited diagnostic value. The latter notoriously progress to serious acute complications (Table 1). The diagnosis is confirmed by direct visualization of the parasite in Giemsastained peripheral blood smears. These deposits typically are seen as small lacunae in silverstained biopsy sections. malaise. which may occur with non-falciparum infections. although a few cases have been recently associated with P. Constitutional manifestations such as headache. 2000 Clinical Profile Malaria is a pyrexial illness that typically begins with a chill. although blood loss may also contribute. This cycle. Anemia and neutrophil leucocytosis are prominent laboratory findings. particularly in endemic areas. the relative preponderance of other causes. patient referral policy. Reported malarial nephropathies in endemic areas. reported figures usually are 25 to 30%. probably depending on the relative impact of different pathogenetic mechanisms. It presents as a steroid-resistant nephrotic syndrome. Fluorescence staining with acridine-orange enhances the diagnostic accuracy of peripheral blood examination.8% of native patients in endemic areas. and associated with other malarial complications. The disease may become chronic if the sporozoan manages to establish a persistent extra-erythrocytic reservoir cycle in the liver. and (2) ARF associated with falciparum malaria in Southeast Asia. and necrosis. P. Postmortem liver biopsy in such cases shows Kupffer cell hyperplasia. Jaundice is the most common association with malarial ARF (MARF). classically complicating quartan malaria.
and interstitial edema and cellular infiltration). and variable degrees of cell necrosis. Proteinuria. The observed elevation of serum antidiuretic hormone (29) does not seem to play a significant role in the pathogenesis of hyponatremia in MARF (1). rhabdomyolysis. and glomerulonephritis (1) (Figure 3). It is attributed to hemolysis.J Am Soc Nephrol 11: 2147–2154. They are characterized by prominent mesangial proliferation with many transit cells. It is attributed to a massive influx of TH1 lymphocytes and is often associated with an acute glomerular lesion. Serum calcium is often reduced out of proportion of the phosphate retention. Acute interstitial inflammation is a well-recognized pattern of malarial nephritis in rodents and after vaccination with P. and basement membrane changes are unusual. The tubular lumen often contain hemoglobin casts. and acidosis. which may be due to hypoparathyroidism of unknown cause (36). Hyperkalemia is striking and often fatal. occurs in 60% of cases (29). Glomerular lesions are detected in approximately one fifth of autopsies on patients with falciparum malaria. Top right: Acute interstitial nephritis. Mesangial matrix expansion is modest. falciparum antigens in monkeys. 2000 Malarial Acute Renal Failure 2151 The effective arterial blood volume is reduced. Unlike the latter. It usually resolves completely with recovery from MARF. The histologic picture in MARF shows a variable mixture of acute tubular necrosis (ATN). A frank SIR syndrome occurs in approximately 5%. persistent proteinuria may be noticed in those who have significant interstitial or glomerular involvement (vide infra). interstitial inflammation is a common histopathologic associated with ATN and acute glomerulonephritis. Although isolated interstitial nephritis has not been reported in humans. red cells in the tubular lumen. ATN is the most consistent histologic finding. reflecting the degree of tissue hypoxia. Bottom left: Proliferative glomerulonephritis. Occasionally. . Although internal dilution is the usual mechanism (vide supra). its incidence and severity correlate with intensity of infection (30). Lactic acidosis is common. Bottom right: Segmental necrotizing glomerulonephritis. and the venules may show clumps of parasitized erythrocytes. However. particularly in the presence of impaired renal function. The interstitium is edematous with a moderate to dense mononuclear cellular infiltration. Top left: Acute tubular necrosis (note the remarkable epithelial disruption. Cerebral malaria is rarely associated with MARF. thereby displaying the three major pathogenetic mechanisms described earlier (vide supra) (Figure 4). reflecting the importance of excessive erythrocyte rosetting as the most important single factor in the pathogenesis of cerebral malaria. being reported in up to 55% of cases. interstitial nephritis. Tubular changes include cloudy swelling. hemosiderin granular deposits. and hypotension occurs on presentation in 20% of cases. Deposition of an eosin- Figure 3. usually less than 1 g/24 h. true sodium wastage that occurs before the onset of oliguria has been reported (1). There are no specific findings in the urinary sediment. Hyponatremia is a typical biochemical finding in MARF. Renal lesions associated with malarial acute renal failure. a patient may progress to acute respiratory distress (1).
younger age and the absence of splenomegaly are associated with higher mortality. and other chemotherapeutics such as mefloquine. a report from India described a reduction of MARF mortality from 75 to 26% when a specialized MARF task force was established in the same institution (37). fibrillar. short acute illness. Malarial antigens occasionally are seen. with a reported mortality of 15 to 45%. the Qinghaosu alkaloids. As mentioned earlier. within the mesangium. The glomerular capillaries often are empty. acute interstitial nephritis. malariae. ophilic granular material has been noticed along the capillary walls.29). or significant jaundice. Segmental necrosis may occur when the capillaries are occluded by erythrocyte rosettes. P. Intravenous quinine remains most widely used in the treatment of cerebral and other serious complications of falciparum malaria. Primaquine is still used in P. benflumetol. Quinine and chloroquine are scarcely removed by dialysis or hemofiltration (1). falciparum strains are chloroquine resistant. acute tubular necrosis. and P. The treatment of ARF usually poses challenging problems Prognosis ARF is a serious complication of malaria. ATN. analogous with an animal model. hepatitis. rial infections may be encountered in patients with MARF. and proguanil administered as monotherapy or in combination. AIN. Interaction of the hemodynamic and immunologic perturbations in the pathogenesis of acute renal disease in falciparum malaria. quinine therapy often leads to hyperinsulinemia. ovale to prevent relapses. Opportunistic pulmonary viral or bacte- . ovale.2152 Journal of the American Society of Nephrology J Am Soc Nephrol 11: 2147–2154. Risk factors for high mortality include late referral. Management Chloroquine used to be the gold standard treatment for malaria. In children. PIGN. which can be avoided by monitoring the blood level and ECG changes. and amorphous material (1. and presentation with oliguria. which contributes to the characteristic hypoglycemia of malignant malaria. or acute respiratory distress have a grave prognosis. Similarly. Patients with severe diarrhea. MPGN. artesunate. multisystem involvement. high parasitemia. 2000 Figure 4. and in the Bowman’s capsule. vivax. hypotension. hence the necessity of monitoring their blood level in patients with prolonged oliguria. Electron microscopy shows subendothelial and mesangial electron-dense deposits along with granular. severe anemia. leading to fatal “black water fever” in severe cases. Immunofluorescence shows finely granular IgM and C3 deposits along the capillary walls and in the mesangium. mesangioproliferative glomerulonephritis. with an increasing frequency in endemic areas. it may induce hemolysis in G6PD-deficient patients. Cardiac toxicity is another important complication of quinine treatment. particularly artemether. most P. Both drugs induce hepatic cytochrome P450. increasing the risk of mortality by their own right. hence the necessity to augment cyclosporine doses in kidney-transplanted patients (38). vivax and P. However. along the glomerular endothelium as well as the medullary capillaries. postinfectious glomerulonephritis (includes exudative and necrotizing variants). Occasional reports from the West suggest that early treatment in well-equipped medical centers may reduce the mortality to nil. Although it remains effective against P. but they may contain a few parasitized red cells or giant nuclear masses in patients who develop intravascular coagulation. Alternative therapies include Fansidar (pyrimethamine ϩ sulfadoxine). and atovaquone.
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