菱田 英里華

Chronic kidney disease (CKD) and hypertension share a complex relationship, each exacerbating the progression of the other. CKD contributes to hypertension by decreasing renal function, leading to fluid retention and increased plasma volume, whereas hypertension exacerbates CKD by increasing glomerular pressure and causing renal damage. This review examines the intertwined nature of CKD and hypertension, exploring the factors driving hypertension in CKD and how hypertension accelerates CKD progression. It discusses the role of the renin-angiotensin system and inflammatory cytokines in this relationship, as well as the potential of blood pressure management to slow renal decline. While studies suggest that meticulous blood pressure control can help attenuate CKD progression, optimal management strategies remain unclear and require further investigation. This review also evaluates the evidence surrounding strict antihypertensive therapy in patients with CKD, considering both diabetic and non-diabetic cases. It recommends blood pressure targets based on CKD stage and presence of diabetes, emphasizing the importance of individualized treatment approaches. Renin-angiotensin system inhibitors are highlighted as a key pharmacological intervention due to their renal protective effects, particularly in patients with CKD with proteinuria. However, evidence regarding their efficacy in patients with CKD but without proteinuria is inconclusive. This review underscores the need for comprehensive approaches to effectively address the intertwined nature of CKD and hypertension and calls for further research to optimize clinical management strategies in this complex interplay.

BACKGROUND: Chronic kidney disease (CKD) and hypertension are significant global health challenges that often coexist and aggravate each other. Renin-angiotensin system (RAS) inhibitors are important to the management of these conditions; however, their efficacy for advanced CKD remains uncertain. SUMMARY: Angiotensin receptor-neprilysin inhibitor (ARNI) have superior efficacy for heart failure (HF) management, as evidenced by landmark trials such as the PARADIGM-HF and PARAGON-HF, thus leading to its endorsement by various guidelines. Although direct evidence supporting the renal-protective effects of ARNI is lacking, post hoc analyses have suggested its potential to mitigate the decline of the estimated glomerular filtration rate and renal events, particularly in patients with HF with a relatively preserved ejection fraction. Mechanistically, ARNI augments the glomerular filtration rate by dilating glomerular arterioles, relaxing mesangial cells, and improving renal medullary blood flow, thereby mitigating interstitial fibrosis progression. ARNI also effectively addresses non-dipper hypertension, particularly in salt-sensitive individuals, thereby reducing the cardiovascular risk. KEY MESSAGES: Uncertainties regarding the efficacy and safety of ARNI for advanced renal failure (estimated glomerular filtration rate <30 mL/min) exist. Excessive hypotension associated with ARNI use may exacerbate the renal function decline, especially in older patients with comorbid HF with a reduced ejection fraction. Hence, vigilant blood pressure monitoring is essential to optimizing the renal benefits of ARNI and minimizing adverse effects. Evidence supporting the renal benefits of ARNI continues to evolve; therefore, ARNI could mitigate renal dysfunction in select patient populations. Further research should be performed to clarify the efficacy of ARNI for advanced renal failure and refine its therapeutic application for patients with concurrent HF and renal dysfunction.

Immunoglobulin A nephropathy (IgAN) is characterized by diverse clinicopathological phenotypes. Herein we present a follow-up study of previously reported identical twin sisters with IgAN. The older sister exhibited more severe kidney histopathology and proteinuria and a lower birthweight than did her younger sister, and only the older sister experienced two childbirths. These raised concerns regarding her kidney outcomes. However, with timely multidisciplinary treatments, the older sister's kidney function remained preserved after 20 years of IgAN history. Our findings indicate the significant contribution of environmental/epigenetic factors to IgAN progression and the need for tailored medical care corresponding to life events.

A 79-year-old male patient with type 2 diabetic nephropathy and hypertension was admitted to our hospital because of acute kidney injury with significantly elevated serum creatinine (8.12 mg/dL) and urinary β2-microglobulin (β2MG, 31,748 μg/L) levels. α-Glucosidase inhibitor (α-GI) miglitol, started two weeks prior to presentation, was discontinued because drug-induced acute interstitial nephritis (AIN) was suspected. Renal biopsy revealed AIN and diabetic nephropathy. The drug-induced lymphocyte stimulation test for miglitol was also positive. After the discontinuation of miglitol, the urinary β2MG levels decreased to the normal range. This case raises the possibility that α-GI miglitol can worsen the renal function in patients with underlying renal dysfunction.

67歳男性。安定した維持透析期に透析困難症をきたし、一過性の意識消失発作を認めたため入院となった。所見では血圧低下を伴う著明な心嚢液貯留が認められ、緊急で心嚢穿刺ドレナージが行われた。その結果、速やかに血圧の回復がみられたが、一方でシャント静脈血管の閉塞が認められたことから、第2病日に経皮的血管形成術が行われた。以後、血液透析を再開し、患者は第11病日に軽快退院となった。尚、本症例における高度の心嚢液貯留は入院2週間前の時点ではみられず、その後、入院となるまでの間に異化亢進を示唆する所見を認めたことから、感冒を契機に相対的な透析量が不足し、透析関連心膜炎を発症したことが示唆された。