Malaria remains a public health problem with significant morbidity and mortality posing major economic and developmental challenges in sub-Saharan Africa . Malarial illness may take a variety of clinical forms, differing in pattern and severity, from uncomplicated to severe malaria. Despite efforts at controlling malaria, two out of ten children admitted to children emergency units suffer from severe forms of malaria and/or its complications . Worldwide, about 90% of the reported cases and 85% of the deaths have been attributed to malaria in sub-Saharan Africa , where Plasmodium falciparum infection is responsible for almost all the morbidity and mortality.
The pathophysiology of severe falciparum malaria is complex and multifactorial with parasitized red blood cell destruction resulting in the release of haemoglobin and other toxic metabolites, up-regulation of cytokines, acute phase reactants all playing important pathogenic roles which may cause inflammation, tubulo-interstitial damage, glomerulonephritis and pigment nephropathy, all of which may lead to acute kidney injury (AKI) . Moreover, previous studies [5, 6] have demonstrated that cardiac output in children with severe malaria is adversely altered, but it is not clear from literature to what extent this alteration affects the kidneys. Data from Ghana  and Kenya  indicated that signs of shock, such as capillary refill, are common in children suffering from severe malaria. These adverse effects, though secondary rather than primary, support potential reversible ischaemic damage to the kidneys during acute malarial illness. Repeated P. falciparum infections can also result in nephron loss leading to chronic renal disease, including nephrotic syndrome, often non-responsive to steroid treatment [9–12].
Though the occurrence of haemoglobinuria and AKI is a significant complication in children with malaria, only a few studies have reported the magnitude. A recent study reported that as many as 19.1% of children with acute falciparum malaria developed haemoglobinuria . AKI has been attributed to malaria in 13.7%  and 46.2%  in Nigeria. Weber et al.  in The Gambia observed that 25% of the cerebral malaria cases and 4% of children with mild malaria had AKI. Mortality from malaria-related AKI could be as high as 23% in endemic area .
Recent studies have shown that cases of severe malaria and its complications are on the increase probably because of the emergence of drug resistant parasites [18, 19]. Early detection and monitoring of effects of malaria on the kidneys are important because timely interventions may prevent progression to irreversible damage. However, this is often very challenging in Africa mainly because of inadequate laboratory facilities. Currently, decisions relating to care of children with acute malaria are mostly guided by physical and biochemistry findings. Apart from the exorbitant cost of biochemistry tests, the turn-around times for getting reports from the laboratory often cause delay in treatments where available. Though ultrasound equipment may be available, sonological assessment of the kidneys in children with malaria is not routinely done, despite the fact that studies have validated the use of ultrasound in assessing renal functions in both clinical and epidemiological studies [20–22]. While other modalities can be used to determine kidney volume [23, 24], ultrasound is preferred in most resource poor settings because it is relatively affordable and non-invasive. It is however, not known whether any change in renal sizes could be detected by using ultrasonographic scanning. This study, therefore, compared the length, width, anterio-posterior diameter and cortical thickness determined using ultrasound as well as estimated volume of kidneys in children with complicated and uncomplicated malaria with those of healthy children with no malaria parasitaemia.