考量到腎臟功能最大化的保留，部分腎臟切除對於治療侷限性的腎臟腫瘤一直以來佔有舉足輕重的地位。為了在手術當下盡可能的減少出血以及保有良好的手術視野，醫師們會以鉗夾短暫性的閉鎖腎臟動脈。正因此步驟導致患側腎臟於手術中短暫性的缺血，使得術後產生急性腎臟損傷也時有所聞。然而，多數患者的急性腎臟損傷會在幾日後恢復，而最終腎臟功能恢復的程度也與手術當下腎臟實質保留的多寡有關。根據過往研究的分析，患者於手術後長期的腎臟功能大多趨於穩定，並且已知術後急性腎臟損傷的程度與患者長期的腎臟功能實則無關。

在老鼠的實驗模型當中，我們得知缺血後的再灌流損傷(ischemia-reperfusion injury)會導致腎臟的纖維化(fibrosis)、腎小管萎縮(tubular atrophy)、以及產生許多腎臟皮質的水泡(cortical cysts)。然而在人體的資料卻少之又少;僅有的文獻告訴我們在接受部分腎臟切除術後的當下，組織學型態的變化不如老鼠實驗模型的劇烈。究竟被保留下來的腎臟實質在幾年之後會發生什麼變化還無從得知。因此我們得以藉由這篇研究來回答這個問題。

這篇回溯性的世代研究主要收錄了來自兩間醫院一共65位因為惡性腎臟腫瘤曾經接受過部分腎臟切除，如今因為腫瘤復發再度接受全腎臟切除的患者。經過作者們的統計分析後發現，多數的患者(72%)可於細胞組織學觀察到惡化的證據，並且有近乎一半的患者(45%)其慢性腎臟病評比的分數(Chronic kidney disease score, CKD score)上升高達3分。而慢性腎臟病評分的上升與手術當中使其缺血的方式與時間無關，也與患者接受部分腎臟切除直至接受全腎上切除的間隔時間無關。唯一與慢性腎臟病評分的上升有關的反而是病患自身的共病(高血壓/糖尿病/慢性腎臟病)。作者們進而比較了”有細胞組織學惡化的患者”與”無細胞組織學惡化的患者”於抽血所顯示的腎臟功能變化，發現兩組雖有細胞組織學惡化程度的不同，但在最終腎功能的表現卻無顯著的差異。

此篇研究與過往的研究結果相同，發現多數的患者在接受鉗夾部分腎臟切除後腎臟功能隨著時間的推移僅有些微的變化。其實我們都知道隨著年紀的老化，腎臟功能本來就會逐年的下降，而當中又以有共病的人們下降的速度較快。然而根據本篇文章的結果，”細胞組織學的變化”與臨床”腎臟功能的變化”無法畫上等號，作者們認為造成兩者變化脫鉤的可能原因來自於本研究觀察的時間不夠久以至於無法觀察到後續長遠的變化，並且推論有顯著細胞組織學變化的這群患者在往後的日子可能會有更顯著的腎功能惡化。又是什麼原因使得慢性腎臟病評分的上升與手術當中使其缺血的方式與時間無關呢?根據過往的研究成果，作者們給出了三個理由: (1)多數的腎臟腎元(nephron) 會在缺血後復原; (2) 腎臟腎元的流失僅是手術後短期內腎功能恢復的重要因子; (3)長時間腎臟功能的下降仍與病人自身的共病有關。

Objective: To compare the histologic chronic kidney disease (CKD) score of renal parenchyma before and years after PN, and to explore factors associated with CKD-score increase and glomerular filtration rate (GFR) decline.

Method: A retrospective review of 147 renal cell carcinoma patients who underwent PN and subsequent radical nephrectomy (RN) due to tumor recurrence was performed in 19 Chinese centers and Cleveland Clinic. Macroscopic normal renal parenchyma was evaluated at least 5 mm away from the tumor in PN specimens and at remote sites in RN specimens.

Results: Sixty-five patients with all necessary data were analyzed. The median interval between PN and RN was 2.4 yr. Median durations of warm ischemia (n = 42) and hypothermia (n = 23) were both 23 min. The histologic CKD score was increased after RN in 47 (72%) patients, with 29 (45%) experiencing more substantial increase (_3). There was no significant difference in the change of CKD score related to the type and duration of ischemia (p = 0.7 and p = 0.4, respectively) or interval from PN to RN (p > 0.9). However, patients with comorbidities of hypertension, diabetes, and/ or pre-existing CKD (hypertension [HTN]/diabetes mellitus [DM]/CKD) demonstrated increased rate and extent of CKD-score increase. On univariate analysis, HTN/DM/CKD was the only predictor of a substantial CKD-score increase (odds ratio: 3.53 [1.12–11.1]). Decline of GFR was modest and similar between patients with/without a substantial CKD-score increase.

Conclusions: Within the context of conventional, limited durations of ischemia, histologic deterioration of preserved parenchyma after PN appears to be primarily due to pre-existing medical comorbidities rather than ischemia. A subsequent decline in renal function was mild and independent of histologic changes.

Patient summary: After clamped PN, the preserved renal parenchyma demonstrated histologic deterioration in many cases, which correlated with the presence of comorbidities such as hypertension, diabetes mellitus, or chronic kidney disease. In contrast, the type and duration of ischemia did not correlate with histologic changes after PN, suggesting that ischemia insult had only limited impact on parenchyma deterioration.