Anemia and Hypoxia Impact on Chronic Kidney Disease Onset and Progression: Review and Updates.

Chronic kidney disease (CKD) is caused by hypoxia in the renal tissue, leading to inflammation and increased migration of pathogenic cells. Studies showed that leukocytes directly sense hypoxia and respond by initiating gene transcription, encoding the 2-integrin adhesion molecules. Moreover, other mechanisms participate in hypoxia, including anemia. CKD-associated anemia is common, which induces and worsens hypoxia, contributing to CKD progression. Anemia correction can slow CKD progression, but it should be cautiously approached. In this comprehensive review, the underlying pathophysiology mechanisms and the impact of renal tissue hypoxia and anemia in CKD onset and progression will be reviewed and discussed in detail. Searching for the latest updates in PubMed Central, Medline, PubMed database, Google Scholar, and Google search engines were conducted for original studies, including cross-sectional studies, cohort studies, clinical trials, and review articles using different keywords, phrases, and texts such as "CKD progression, anemia in CKD, CKD, anemia effect on CKD progression, anemia effect on CKD progression, and hypoxia and CKD progression". Kidney tissue hypoxia and anemia have an impact on CKD onset and progression. Hypoxia causes nephron cell death, enhancing fibrosis by increasing interstitium protein deposition, inflammatory cell activation, and apoptosis. Severe anemia correction improves life quality and may delay CKD progression. Detection and avoidance of the risk factors of hypoxia prevent recurrent acute kidney injury (AKI) and reduce the CKD rate. A better understanding of kidney hypoxia would prevent AKI and CKD and lead to new therapeutic strategies.

Effects of Nondipping Blood Pressure Changes: A Nephrologist Prospect.

Blood pressure (BP) variations depend on various internal, environmental, and behavioral factors. BP fluctuations occur both in normotensive and hypertensive people. Although it fluctuates over the 24-hr day and night, the morning BP increases after waking up and declines throughout sleep. It is typical for BP to decrease by 10% to 20%, while sleeping, known as dipping BP. However, if there is no decrease in nighttime mean systolic BP or a drop of less than 10 mmHg, it is called nondipping BP. Conversely, reverse dipping BP means an increase in mean systolic BP instead of a drop during the night. Reverse dipping is observed in hypertension (HTN), diabetes mellitus (DM), chronic kidney disease (CKD), and obstructive sleep apnea (OSA) syndrome. The introduction of ambulatory BP monitoring (ABPM) led to the emergence of identifying normal and elevated BP patterns. Non-dipping BP increases the risk of cardiovascular system (CVS) complications such as left ventricular hypertrophy, proteinuria, glomerular filtration rate (GFR) reduction, and CKD progression. A loss or blunting of the normal BP profile is recognized as a deleterious variant, and restoring abnormal BP patterns has been reported to significantly impact end-organ damage, morbidity, and mortality. In this non-systematic clinically-oriented, comprehensive review, we aim to update the BP variables and the pathophysiology of nondipping BP and point out the areas which need more investigation from a nephrology perspective because the nondipping BP increases the risk of proteinuria, GFR reduction, and CKD progression. A literature search of PubMed, Google, EMBASE, and Google Scholar was conducted. Checks of selected papers and relevant reviews complemented the electronic search. With improved BP measurement methods, the physiology of BP profile variations is readily detectable during the day and night. A nondipping BP profile is a distinct BP pattern that may have significant end-organ damage effects and therapeutic importance for nephrologists. The pathophysiology of the nondipping BP variant must be clarified to prevent complications, and further investigations are required. Furthermore, there is debate about the best BP index to utilize: systolic BP, diastolic BP, mean arterial pressure, or a mixture of all. All these areas are important and need new research projects.

Malignancy diseases and kidneys: A nephrologist prospect and updated review.

Acute kidney injury (AKI), chronic renal failure, and tubular abnormalities represent the kidney disease spectrum of malignancy. Prompt diagnosis and treatment may prevent or reverse these complications. The pathogenesis of AKI in cancer is multifactorial. AKI affects outcomes in cancer, oncological therapy withdrawal, increased hospitalization rate, and hospital stay. Renal function derangement can be recovered with early detection and targeted therapy of cancers. Identifying patients at higher risk of renal damage and implementing preventive measures without sacrificing the benefits of oncological therapy improve survival. Multidisciplinary approaches, such as relieving obstruction, hydration, etc., are required to minimize the kidney injury rate. Different keywords, texts, and phrases were used to search Google, EMBASE, PubMed, Scopus, and Google Scholar for related original and review articles that serve the article's aim well. In this nonsystematic article, we aimed to review the published data on cancer-associated kidney complications, their pathogenesis, management, prevention, and the latest updates. Kidney involvement in cancer occurs due to tumor therapy, direct kidney invasion by tumor, or tumor complications. Early diagnosis and therapy improve the survival rate. Pathogenesis of cancer-related kidney involvement is different and complicated. Clinicians' awareness of all the potential causes of cancer-related complications is essential, and a kidney biopsy should be conducted to confirm the kidney pathologies. Chronic kidney disease is a known complication in malignancy and therapies. Hence, avoiding nephrotoxic drugs, dose standardization, and early cancer detection are mandatory measures to prevent renal involvement.

IgA nephropathy pathogenesis and therapy: Review & updates.

BACKGROUND: IgA nephropathy (IgAN) is the most frequent type of primary glomerulonephritis since the first type was described more than four decades ago. It is the prevalent cause of primary glomerular disease that causes end-stage renal disease. In most patients with IgAN, hematuria is the most common reported symptom, particularly in those with a preceding upper respiratory tract infection. Although the pathogenesis of IgAN is usually multifactorial, autoimmune complex formation and inflammatory processes are the most widely recognized pathogenic mechanisms. Multiple approaches have been trialed as a therapy for IgAN, including tonsillectomy, steroids, other immune-suppressive therapy in different regimens, and kidney transplantation. AIM AND METHOD: PubMed, Google, Google Scholar, Scopus, and EMBASE were searched by the authors using different texts, keywords, and phrases. A non-systemic clinical review is intended to review the available data and clinical updates about the possible mechanism(s) of IgAN pathogenesis and treatments. CONCLUSION: IgAN has a heterogeneous pattern worldwide, making it difficult to understand its pathogenesis and treatment. Proteinuria is the best guide to follow up on the IgAN progression and treatment response. Steroids are the cornerstone of IgAN therapy; however, other immune-suppressive and immune-modulative agents are used with a variable response rate. Kidney transplantation is highly advisable for IgAN patients, although the recurrence rate is high. Finally, IgAN management requires collaborative work between patients and their treating physicians for safe long-term outcomes.

Fasting Ramadan in Chronic Kidney Disease (CKD), Kidney Transplant and Dialysis Patients: Review and Update.

Chronic kidney disease (CKD) is a common disease in the Islamic regions. Dehydration occurs after prolonged fasting, particularly in hot and humid climates. In the Arabic months' calendar, Ramadan is a month of maximum given deeds, where Muslims are required to fast from dawn till sunset. Depending on where you live and when the Ramadan month falls, fasting might last anywhere from 10 to 20 hours or more. In certain circumstances, such as poorly controlled diabetes and advanced CKD patients who are allowed to break their fast, the Ramadan fasting amendment is viable. Some Muslims, however, continue fasting despite these circumstances, placing themselves at risk, which is not allowed in the Islamic religion. There are no medical recommendations that specify who should and should not fast. Nonetheless, the recommendations have been extracted from several published studies. The authors searched EMBASE, PubMed, Google Scholar, and Google for publications, research, and reviews. All authors debate and analyze the related articles. Each author was assigned a part or two of the topics to read, study, and summarize before creating the final draft of their given section. Then this comprehensive review was completed after discussion sessions. In conclusion, by the Islamic religion view, fasting Ramadan is mandatory for every wise adult person. People who have chronic diseases or that may deteriorate by fasting are exempted from fasting. It seems that fasting and the associated disease hours are determinant factors to fasting or not fasting. Up to our knowledge, there are no established guidelines for CKD patients and physicians to follow; however, the International Diabetes Federation and Diabetes and Ramadan (IDF-DAR) Practical Guidelines 2021 have been issued for CKD diabetic patients and fasting.

Blood Pressure and Chronic Kidney Disease Progression: An Updated Review.

Hypertension (HTN) is common in chronic kidney disease (CKD), and it may aggravate CKD progression. The optimal blood pressure (BP) value in CKD patients is not established yet, although systolic BP ≤130 mmHg is acceptable as a target. Continuous BP monitoring is essential to detect the different variants of high BP and monitor the treatment response. Various methods of BP measurement in the clinic office and at home are currently used. One of these methods is ambulatory BP monitoring (ABPM), by which BP can be closely assessed for even diurnal changes. We conducted a non-systematic literature review to explore and update the association between high BP and the course of CKD and to review various BP monitoring methods to determine the optimal method for BP recording in CKD patients. PubMed, EMBASE, Google, Google Scholar, and Web Science were searched for published reviews and original articles on BP and CKD by using various phrases and keywords such as "hypertension and CKD", "CKD progression and hypertension", "CKD stage and hypertension", "BP control in CKD", "BP measurement methods", "diurnal BP variation effect on CKD progression", and "types of hypertension." We evaluated and discussed published articles relevant to the review objective. Before preparing the final draft of this article, each author was assigned a section of the topic to read, research deeply, and write a summary about the assigned section. Then a summary of each author's contribution was collected and discussed in several group sessions. Early detection of high BP is essential to prevent CKD development and progression. Although the latest Kidney Disease Improving Global Outcomes (KDIGO) guidelines suggest that a systolic BP ≤120 mmHg is the target toprevent CKD progression, systolic BP ≤130 mmHg is universally recommended.ABPM is a promising method to diagnose and follow up on BP control; however, the high cost of the new devices and patient unfamiliarity with them have proven to be major disadvantages with regard to this method.