Urolithiasis (UL) is increasingly prevalent due to rising cardiorenometabolic diseases, posing significant management challenges despite advances in urological techniques. Sodium-glucose cotransporter-2 (SGLT2) inhibitors, primarily used for type 2 diabetes mellitus, chronic kidney disease, and heart failure, have emerged as a potential novel approach for UL treatment. These inhibitors may help reduce the risk of urolithiasis, particularly in patients with diabetes, by improving glycemic control and altering urinary chemistry, which are crucial factors in stone formation. However, the changes in urinary composition induced by SGLT2 inhibitors might also increase the risk of uric acid stone formation. This review evaluates the potential of SGLT2 inhibitors in managing UL, highlighting both the benefits and the risks. While these inhibitors show promise in reducing new and recurrent urinary stones in patients with diabetes, data on their effects in patients without diabetes who form stones are limited. Current human evidence largely comes from post hoc analyses of randomized controlled trials (RCTs) and large-scale database studies, with only one study providing detailed stone composition data. Experimental studies in animal models and cell lines have focused on calcium oxalate (CaOx) stones, showing that SGLT2 inhibitors specifically target CaOx stone formation and related renal inflammation. Although primarily studied for CaOx stones, their potential impact on other calcium-containing stones, such as calcium phosphate, remains promising. Further research is needed to explore their therapeutic potential and optimize treatment strategies.

Urolithiasis is a highly prevalent and multifactorial disease, representing the most common urological condition globally. Its incidence continues to rise, posing a significant public health challenge. Management strategies are tailored to individual patients, considering factors such as stone size, composition, location, and underlying metabolic conditions. This review provides a comprehensive overview of both pharmacological and surgical approaches to urolithiasis, emphasising recent advancements and emerging technologies. Surgical treatments, particularly minimally invasive procedures, have shown considerable improvement, offering highly effective solutions with reduced morbidity. While surgical interventions are essential, pharmacological therapies play a key role in preventing recurrence and addressing metabolic abnormalities that contribute to stone formation. Advances in understanding the molecular mechanisms and pathophysiology of urolithiasis are crucial for developing targeted therapies. A holistic approach that integrates advanced surgical techniques with pharmacological interventions, tailored to individual metabolic profiles, is essential for optimising patient outcomes. Personalised management, supported by regular monitoring of urinary pH, metabolic profiles, and adherence to treatment regimens, is vital to reducing recurrence and improving the quality of life for patients with urolithiasis.

Background/Objectives: Hepatocyte growth factor (HGF) is a protective factor against acute renal injury and chronic renal fibrosis. A positive correlation between HGF and blood pressure (BP) has been established. This study aimed to determine the association between serum HGF concentration and albuminuria in subjects with optimal blood pressure (OBP) and untreated arterial hypertension (UAH), as well as its association with BP levels, serum glucose levels, and inflammatory markers. Methods: Data from 563 subjects were analyzed. Albuminuria was normalized to urine creatinine and expressed as the albumin/creatinine ratio (ACR). HGF, serum glucose, C-reactive protein, and blood leucocyte counts were measured. BP was measured and subjects were divided into optimal blood pressure (BP < 120/80 mmHg, N = 295) and untreated arterial hypertension (BP > 140/90 mmHg, N = 268) groups. Results: The subjects with UAH were significantly older and had higher values of body mass index, waist circumference, serum total and LDL cholesterol levels, triglyceride levels, fasting glucose levels, and ACR (all p < 0.001). A significant positive correlation was found between serum HGF concentration and ACR in both groups. There was no difference or correlation between HGF and BP or inflammatory markers in either group. The multivariate regression analysis identified serum HGF concentration as a strong predictor of ACR increase (Beta = 0.376, p < 0.001). Conclusion: This study found that serum HGF concentration is associated with albuminuria not only in individuals with untreated arterial hypertension, but also in those with optimal blood pressure. The results suggest that serum HGF is an independent predictor of ACR increase in both groups.

We report the case of 39-year-old Caucasian man presenting in emergency department with new onset of severe hypertension with hypokalaemia eight weeks after renal colic. Patient was referred to a hypertension unit for further investigation. Hormonal analysis confirmed secondary aldosteronism and slightly impaired kidney function. Imaging revealed smaller right kidney, ‘string of beads appearance’ of distal part of right renal artery, a short zone of dissection and renal infarction. Renal scintigraphy showed significant blood flow reduction and severe functional damage of the right kidney. Despite multidrug antihypertensive treatment patient's hypertension was resistant and target organ damage evolved. After initial patient's refusal, he was later successfully treated with laparoscopic simple nephrectomy. Histopathological analysis confirmed renal artery dissection and medial fibroplasia. Thereafter, hypertension was controlled with trandalopril monotherapy. This is a first case report of the patient with renovascular multifocal fibromuscular dysplasia, dissection and renal infarction whose diagnosis of the disease was confirmed by angiography and histopathologic analysis. Resistant hypertension was successfully treated with nephrectomy.