Received: 10-Nov-2022, Manuscript No. IJMAR-22-83632; Editor assigned: 14-Nov-2022, Pre QC No. IJMAR-22-83632 (PQ); Reviewed: 05-Dec-2022, QC No. IJMAR-22-83632; Revised: 13-Dec-2022, Manuscript No. IJMAR-22-83632 (R); Published: 21-Dec-2022, DOI: 10.15651/IJMAR.22.3.015
Malaria is an infectious disorder of exceptional hobby for Public Health as it stays because the maximum regular endemic disorder in the world. The etiologic agents are parasitic protozoans of the genus Plasmodium. There are 4 malarial species i.e., P. falciparum, P. vivax, P. ovale and P. malaria. Which have a tendency to be a greater extreme disorder is P. vivax, P. ovale, tertian malaria, and P. malariae causes quartan malaria. Clinical manifestations of kidney involvement in malaria encompass proteinuria, micro albuminuria and urinary casts, said in 20 to 50% of cases. Nephrotic syndrome has additionally been defined with inside the contamination through the means of P. falciparum, however it's far rare. This paper highlights the primary components of kidney involvement in malaria and maximum current studies addressing this issue.
AKI is a known complication of malaria and can occur in approximately 40% of severe Plasmodium falciparum patients in endemic areas, contributing to the high mortality rate of approximately 75% of cases. Plasmodium falciparum causes the most severe forms of malaria and is responsible for most Acute Kidney Injury (AKI). Malaria was the first parasitic infection positively associated with glomerular disease in tropical regions. Severe malaria can cause disease in glomeruli, tubules, and interstitial regions. Kidney disease in malaria is primarily due to red blood cell abnormalities. Parasitic erythrocytes tend to adhere to healthy erythrocytes, platelets, and capillary endothelium, leading to the formation of rosettes and thrombi that impair microcirculation. These events may contribute to renal injury associated with hemodynamic instability such as hypovolemia and shock.
Glomerulonephritis in patients infected with Plasmodium falciparum is uncommon and children seem more likely to be affected by this complication. Mild proteinuria, microalbuminuria, and casts have been reported in 20%-50% of cases. Nephrotic syndromes associated with Plasmodium falciparum infections are rare. This type of infection is associated with acute tubular necrosis, cast nephropathy, inflammatory stromal infiltration and edema. In malaria, the mechanisms leading to AKI are complex, involving mechanical and immune factors, cytokine release, and acute-phase responses. AKI may present as a component of multiple organ failure or as a single complication. In general, the prognosis for the latter is good. Several virulence mechanisms interact for clinical manifestations. The predominant lesions are acute tubular necrosis and mild proliferative glomerulonephropathy.
Although the pathogenic mechanisms of AKI in malaria are not yet fully defined, pathological processes such as parasite shedding, endothelial dysfunction, oxidative stress and immune-mediated injury may converge on the kidney. There are several. One of the hallmarks of malaria infection is intravascular hemolysis, primarily of Plasmodium-Infected Red Blood Cells (pRBCs), leading to the release of cell-free heme and host- and parasite- derived molecules that potently induce inflammatory responses. Some degree of intravascular hemolysis occurs in all parasite species, but the most extensive hemolysis occurs in Plasmodium falciparum infection as a result of the higher parasite density normally found in the blood of this parasite species.
Hyperkalemia, on the other hand, is secondary to hemolysis, acidosis, and rarely rhabdomyolysis. Anemia and thrombocytopenia are primarily due to malaria infection. However, when a patient develops her TMA, anemia and thrombocytopenia may worsen over time. Patients with malaria AKI may develop proteinuria due to glomerulonephritis. In particular, complement activation has been implicated in the pathogenesis of malaria AKI, although complement levels are usually normal. If a patient develops oliguric AKI, treatment should begin with supportive care and avoid fluid boluses unless the patient has severe hypotension. Renal replacement therapy should be considered early and initiated when supportive care is inadequate. There is no consensus on the preferred dialysis modality, and available resources should determine which modality to use.