Renal Affection in Philadelphia Negative Myeloproliferative Neoplasms | ||||
| Al-Azhar International Medical Journal | ||||
| Volume 2024, Issue 5, May 2024 | ||||
| DOI: 10.58675/2682-339X.2429 | ||||
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| Authors | ||||
| Youssef Eissa1; Ahmed Abdelaziz2; Youssef Nassar1; Mohamed Alagouz3 | ||||
| 1Internal Medicine, Faculty of Medicine for Boys, Al-Azhar University, Cairo, Egypt | ||||
| 2clinical Pathology _faculty of medicine Al-Azhar university Cairo, Egypt | ||||
| 3Internal Medicine, Faculty of Medicine, Al-Azhar University, Cairo, Egypt | ||||
| Abstract | ||||
| Background: Rare clonal neoplastic illnesses of the myeloid hematopoietic stem cells (HSC) that might impact other body systems are known as classical Philadelphia chromosome-negative myeloproliferative neoplasms (MPN). Aim and objectives: To assess the frequency of renal affection in myeloproliferative neoplasms that are Philadelphia negative. Patients and methods: A prospective study that includes 60 patients (their age above 18 years old) with Aphiladelphia negative myeloproliferative neoplasms to asses renal affection by history taking, clinical evaluation, laboratory evaluation, and pelvis. The US. From January 2023 to December 2023. All patients will be selected from the Internal Medicine Department (at both Al Hussein and Cairo University Hospitals) and outpatient clinics, with appropriate consent to participate in this study. Results: There were statistically significant elevations in B. urea, Uric acid, alb. Creat. The ratio in patient groups (Where p values are 0.001 >, 0.003, and 0.001 > respectively), with a statistically significant reduction in GFR (P value 0.01). Interestingly, there was no significant difference in s—creatinine levels (0.07). Urinary albumin excretion and Urinary Uric acid excretion were significantly higher in patient groups. In all instances, the PMF group experienced the most impressive change. Conclusion: Increased JAK2 mutant allele burden in MPN patients is associated with a greater risk of CKD and adverse dynamics of renal function over time. These findings provide credence to the hypothesis that the biology of MPN disease may have a role in the declining kidney function seen in a significant proportion of MPN patients. | ||||
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