## 1 Introduction  
Diabetes mellitus (DM) is a chronic systemic metabolic disorder characterized by hyperglycemia and metabolic alterations [1]. DM is characterized by fasting glucose \(\geq\) 7.0 mmol/L (126 mg/dL) or random blood glucose levels of \(\geq\)11.1 mmol/L (200 mg/dL) [2]. The International Diabetes Federation estimates that DM affects 415 million people worldwide, which is expected to increase to 642 million people by 2040 [3].  
Renal dysfunction is a common occurrence in DM, and around 44% of new cases of chronic kidney disease are diagnosed in diabetic patients [4]. The presence of renal complications in DM patients significantly increases the mortality rates when compared with DM patients without renal complications [5, 6]. However, the precise mechanism by which the renal dysfunction increases the mortality in diabetic patients remains poorly characterized [7].  
Hyperglycaemia in DM can induce pathophysiological changes in the kidneys, including dysfunction of cellular responses to high glucose levels, alterations in renal vasculature, and surrounding tissues including glomeruli and podocytes [8]. Excess glucose can lead to advanced formation of glycation end (AGE) products [9, 10], which bind to the basement membrane and induce the release of pro-inflammatory cytokines, resulting in interstitial fibrosis and glomerulosclerosis [11; 12]. AGE can also cause hypertrophy and excessive proliferation of cells, leading to an increase in the number and size of tubular and glomerular epithelial cells [13]. In general, DM leads to an increase in glomerular volume [14; 15], along with characteristic vascular changes such as hyalinosis of the afferent and efferent arterioles and thickening of the walls of the renal arteries [16].  
Currently, the management strategies of DM involve standard treatments such as insulin therapy and antidiabetic drugs [17; 18; 19]. However, these treatments have certain drawbacks, such as reduced effectiveness with oral administration, relatively short storage time, fatal side effects of hypoglycaemia due to overdosing, and discomfort due to injection needles [20]. Standard drugs also carry several other adverse side effects resulting in poor compliance by the patients [20].  
_Annona muricata_, also known as soursop leaf, is known for its antidiabetic effects [21; 22; 23; 24]. _A. muricata_ is a plant that comes from the Annonaceae family [25]. The leaf, seed, and fruit extracts of _A. muricata_ are often used in herbal medicine [26]. Those extracts from this plant inhibit glucose absorption by suppressing hydrolytic enzymes such as \(\alpha\)-amylase and \(\alpha\)-glucosidase [21]. Several studies have shown antihypertensive, vasodilator, anticancer, and antidepressant effects from this plant [27; 28; 29]. Moreover, [PERSON] and co-workers demonstrated the effect of _A. muricata_ extract on the lipid profile, kidney, and liver function in a mouse model of DM induced with Streptzootcin [30]. In that study, there was a significant increase in HDL cholesterol, a reduction in serum creatinine indicating improved renal function, and reduced serum AST and ALT enzymes indicating enhanced liver function following the administration of _A. muricata_ plant extract [31]. Another study by [PERSON] et al. also showed that _A. muricata_ leaf extract had an inhibitory effect on \(\alpha\)-amylase and \(\alpha\)-glucosidase, which outperformed the current standard antidiabetic drugs, namely acarbose and metformin [21].  
However, no study has characterized a direct effect of the ethanol extract of _A. muricata_ leaves on renal morphology, especially related to the proliferation and growth of the glomerulus, the Bowman's space, and the proximal tubular convolution, which are among the sites primarily affected in DM patients. We aimed to fill this gap in the literature by determining the effect of the ethanol extract of _A. muricata_ leaves on renal histopathology of Swiss Webster mice with alloxan-induced diabetes.