Climate change significantly impacts natural environments, economies, and human health, with rising global temperatures causing increasingly frequent extreme weather events. Studies have shown that heat exposure accelerates kidney function decline and increases hospitalizations for renal diseases. Heat contributes to kidney disease through mechanisms such as dehydration, ischemic injury, inflammation, and oxidative stress, leading to acute kidney injury, chronic kidney disease, increased risk of kidney stone formation, and proteinuria. In light of the anticipated rise in temperatures in the forthcoming years, it is of crucial importance to know the possible consequences for kidney health. This review highlights the relationship between these phenomena, the potential complications that may arise, and the mechanisms of their occurrence. The identification of these mechanisms will further support the development of future targeted preventive strategies and interventions.

Nephrotoxicity is a common complication during antineoplastic therapy, particularly when platinum-based medications are used. Early detection of this condition is crucial for improving risk stratification and management, thereby enhancing decision-making in kidney disease treatment. However, traditional biomarkers for renal assessment lack sensitivity in identifying early or subclinical damage, underscoring the need for novel and more precise markers. This study aimed to investigate the effectiveness of urinary KIM-1, clusterin, nephrin, and serum cystatin C in detecting nephrotoxicity associated with platinum-based therapies. A total of 43 patients with different oncological diseases participated in the prospective study, divided into two groups based on the nephrotoxic potential of the administered drugs: patients treated with cisplatin (high-risk group for nephrotoxicity) and patients treated with oxaliplatin/carboplatin (low-to-moderate risk group for nephrotoxicity). The results showed that nephrotoxicity, determined as a decrease in eGFR of >10 mL/min/1.73 m² at the sixth month after initiation of platinum-based therapy, occurred in 54.3% of cases, with 80% of these attributable to cisplatin-based therapy. Conventional renal biomarkers, such as the serum creatinine and urine albumin-creatinine ratio, have shown controversial results in the course of the study. In contrast, the patients treated with cisplatin, as well as those who developed nephrotoxicity, showed significant increases in the mean values of cystatin C (p < 0.001, respectively, p < 0.001), urinary KIM-1 (p = 0.005, respectively, p = 0.002), and urinary clusterin (p = 0.001, respectively, p = 0.001). Among the group with a low to moderate risk of nephrotoxicity including those treated with oxaliplatin/carboplatin, no statistically significant changes over time were observed in any of the biomarkers. These findings suggest that the aforementioned biomarkers can be used for the early detection of cisplatin-induced eGFR decline.

Background and Clinical Significance: Spontaneous renal hematoma, also known as Wunderlich syndrome (WS), is a rare disease characterized by the acute onset of spontaneous renal hemorrhage into the subcapsular, perirenal, and/or pararenal spaces without a history of prior trauma. WS can be a life-threatening condition due to hemorrhagic shock; consequently, prompt diagnosis and a therapeutic approach are essential for favorable outcomes. Treatment ranges from conservative management to surgical intervention. The most common etiologies are neoplasms and vascular diseases, but WS can also be observed in patients undergoing hemodialysis. In patients with end-stage renal disease (ESRD), especially those on hemodialysis, acquired cystic kidney disease and renal cell carcinoma are among the primary causes of WS. Although less common, WS can develop in dialysis patients even in the absence of traditional (primary) risk factors. In general, patients with chronic kidney disease (CKD) have a paradoxical hemostatic profile, likely explaining their higher tendency to bleed, so WS can occur without existing predisposing factors. The multifactorial pathogenesis in these patients includes functional platelet abnormalities, intimal arterial fibrosis, chronic inflammation, and oxidative stress associated with ESRD. The use of hemodialysis-related antithrombotic medications could serve as another contributing factor increasing the risk of bleeding. C ase Presentation: We present a case report of a 62-year-old male on chronic dialysis who developed sudden right-sided lumbar pain and hematuria during dialysis without evidence of prior trauma. Imaging revealed a large subcapsular hematoma of the right kidney. Further investigations did not reveal additional risk factors in this instance; however, his routinely used hemodialysis-related antithrombotic medications were potentially a contributing factor. Despite conservative treatment, his condition worsened, and the hematoma enlarged, requiring emergency nephrectomy. Postoperatively, his condition gradually improved. Conclusions: This case highlights the importance of considering WS in hemodialysis patients, even without the presence of traditional risk factors, as well as including WS in the differential diagnosis of acute abdominal pain.

Background and Clinical Significance: Spontaneous renal hematoma, also known as Wunderlich Syndrome (WS) is a rare disease, characterized by the acute onset of spontaneous renal hemorrhage into the subcapsular, perirenal, and/or pararenal spaces, without a history of prior trauma. It can be a life-threatening condition due to hemorrhagic shock, consequently, prompt diagnosis and therapeutic approach are essential for favorable outcomes. Treatment ranges from conservative management to surgical intervention. The most common etiologies are neoplasms, vascular diseases but it can be also observed in patients undergoing hemodialysis, especially those with acquired cystic kidney disease or renal cell carcinoma. However, patients with CKD, on particular those on dialysis, have a paradoxical hemostatic potential with increased rates of bleeding, so WS may occur even without the so-called common risk factors. The multifactorial pathogenesis in these patients includes specific coagulation abnormalities and the impaired architectonics of the renal tissue, as well as the use of antithrombotic agents. Case Presentation: We present a case report of a 62-year-old male on chronic dialysis who developed a sudden right-sided lumbar pain and hematuria during dialysis without evidence of prior trauma. Imaging revealed a large subcapsular hematoma of the right kidney. Despite conservative treatment, his condition worsened and the hematoma enlarged, requiring emergency nephrectomy. Pathology confirmed extensive hemorrhage in a nephrosclerotic kidney. Postoperatively, his condition gradually improved. Conclusions: This case highlights the importance of considering WS in hemodialysis patients, and should be included in differential diagnosis of acute abdominal pain.

The term “steinstrasse” was first introduced by Egbert Schmiedt and Christian Chaussy in the 1980s to describe stone accumulation in the ureter following extracorporeal shock wave lithotripsy. Clinically, patients present with lumbar pain, nausea/vomiting, and lower urinary track symptoms. Severe cases may lead to obstruction or sepsis. It is observed mostly in patients who have undergone extracorporeal shock wave lithotripsy, but in rare cases it can occur spontaneously. Spontaneous formation of steinstrasse is a rare phenomenon with only several cases reported in literature so far and for that reason there are no standard protocols for the management of such patients. Various factors need to be taken into account when choosing the optimal therapeutic strategy. We present a rare clinical case of idiopathic spontaneously occurring steinstrasse. We will discuss the clinical course, the diagnostic algorithm, and the therapeutic approach.

Background and Objectives: Hyperphosphatemia is a key component of chronic kidney disease-mineral and bone disorder and is associated with higher rates of cardiovascular events and mortality in patients undergoing dialysis. Phosphate binders are essential for phosphorus reduction, and their evaluation relies on several factors, such as chemical composition, binding capacity, and safety profile. Unfortunately, long-term management is hindered by high pill burden and poor adherence. Magnesium phosphate binders have proven effectiveness in reducing phosphate levels. Nevertheless, despite their efficacy, they are not widely used in clinical settings because of concerns related to their use. This study assessed the efficacy of low-dose magnesium carbonate as a phosphate binder in patients undergoing chronic dialysis, focusing on its biochemical control, tolerability, and cost-effectiveness. Materials and Methods: A prospective observational study was conducted on 54 hemodialysis patients with end-stage renal disease at a single dialysis center. Patients were taking either 250 mg magnesium carbonate or 2400 mg sevelamer carbonate for 3 months. Results: Both groups showed decreased phosphorus levels, with a 14.2% significant reduction in the magnesium carbonate group (p < 0.001) and a 5.1% reduction in the sevelamer carbonate group. At the end of the study, no significant differences were observed between the groups (p = 0.682). In the magnesium carbonate group at month 3, compared to baseline, no significant differences were detected in other laboratory parameters reflecting calcium–phosphorus metabolism (Ca—p = 0.681, PTH—p = 0.126). Simultaneously, good compliance without clinically relevant gastrointestinal side effects was observed, including the absence of clinically significant hypermagnesemia. Conclusions: The phosphorus-lowering potential of low-dose magnesium carbonate is non-inferior to that of low-dose sevelamer carbonate. However, its favorable safety profile, low incidence of adverse effects, and cost-effectiveness make it a promising option in clinical practice, further highlighting the need for better recognition by physicians.