1. Top of page

The current trend towards nephron-sparing partial nephrectomy for renal tumours, and the rapid expansion of the laparoscopic approach for this purpose, has resurrected a clinical issue: the hazards of renal ischaemia needed to obtain a bloodless field for meticulous dissection and reconstruction of the kidney. A quarter of a century ago, when complex nephrolithotomies were the only therapeutic solution for many ‘staghorn’ stones, this was a topic dominating experimental and clinical interest. Present-day statements such as ‘mean warm ischaemia of 43 ± 10 min did not adversely impact renal function in laparoscopic partial nephrectomy’ (as determined mainly by serum creatinine in the presence of a contralateral kidney) [1] or ‘the impact of repeated clamping of the renal artery has never been studied in a larger animal model’[2] show the deficiency of modern systems for tracking earlier reports. They seem to become blurred on publications before 1985. By contrast, we older urologists tend to see the past clearly, and the present as hazier. As subjective as this view might be, it calls for a senior urologist to speak out to avoid going through the pain of re-inventing history.

The sequelae of temporary renal ischaemia with the normothermic kidney remaining in situ were extensively studied in the late 1970s and early 1980s [3]. The question of how long normothermic ischaemia is tolerated without permanent damage is best documented in the control groups of studies attempting to prevent ischaemic damage by specific protective means [3,4]. Porcine kidneys resemble those of humans most closely in renal morphology and physiology; 60 min of occlusion of the renal artery resulted in a mean 62% decrease of 3H-inulin clearance and a mean 35% decrease of 125I-hippuran clearance 24 h later. This functional loss was considerably more pronounced than after 30 min of warm ischaemia, yet not different from that after 90 min, indicating that the onset of irreversible changes is somewhere at 30–60 min [5]. The most convincing data come from morphological studies on human kidneys. Rocca-Rossetti et al. [6] studied 30 kidneys removed after 15–60 min of warm ischaemia. Ultra-thin sections using light and electron microscopy showed distinct changes, appearing mainly in the proximal tubules after ≈ 20 min, with rapidly increasing signs of cellular degeneration at ≥ 30 min, and complete cellular degeneration at all levels of the nephron at ≥ 60 min. In pre-damaged kidneys, such as from pyelonephritis or chronic obstruction, tolerance to ischaemia was even lower [6]. Despite compensatory hypertrophy, solitary kidneys are not privileged kidneys in terms of ischaemic tolerance [7]. Clinical tests for measuring renal function are cruder, and early damage might be repaired or compensated over time. Nevertheless, based on data such as these and a wealth of clinical experience in complex nephrolithotomies, it became the accepted standard to limit normothermic ischaemia without specific protective measures to 30 min at most [8].

Renal perfusion, both before and after ischaemia, has a profound impact on the ischaemic tolerance of the kidney. Hypotension, insufficient hydration and/or arterial vasospasm resulting from traumatic dissection of the renal artery augment ischaemic damage [9]. Even after a short ischaemic challenge, the re-flow phase is characterized by regional malperfusion, and even ‘no-flow’ phenomena in the deeper cortex [10].

Intermittent vs continuous renal arterial occlusion potentiates these effects and hence renal damage [11]. Bulk clamping of the renal pedicle, rather than just the renal artery, carries the inherent risk of incomplete arterial yet complete venous occlusion, with an additional derangement of post-ischaemic haemodynamics. Moreover, it comes at a higher risk of slipping of the clamp and intimal damage to the renal artery.

In essence, therefore, experience from stone surgery in renal ischaemia clearly implies:

  • • 
    the patient must be well hydrated and haemodynamically stable before clamping the renal artery;
  • • 
    the renal artery should be occluded directly after careful atraumatic dissection, and the renal vein only when needed (avoiding pedicle clamping);
  • • 
    intermittent or incomplete occlusion of the renal artery are to be avoided;
  • • 
    normothermic ischaemia of the kidney is to be restricted to 30 min at most; if longer ischaemia is anticipated, special protective measures are needed (hypothermia).

Nephrolithotomies have become historical procedures and much of the experimental evidence for developing these rules might have been obtained with methods outdated today. Nevertheless, it is difficult to understand why these rules should not also apply for laparoscopic nephron-sparing surgery. Until clearly proven otherwise by hard data, rather than ‘not having been investigated in recent studies’ they still appear to be fully valid.


  1. Top of page
  • 1
    Kane CJ, Mitchell JA, Meng MV, Anast J, Carroll PR, Stoller ML. Laparoscopic partial nephrectomy with temporary arterial occlusion: description of technique and renal functional outcomes. Urology 2004; 63: 2416
  • 2
    Orvieto MA, Mendiola FP, Gong ER et al. Ischemia preconditioning does not increase resilience to warm ischemia in a solitary porcine kidney model. J Endourol 2006; 20 (Suppl. 1): A72
  • 3
    Marberger M, Dreikorn K eds., Renal Preservation. Baltimore-London: Williams & Wilkins, 1983
  • 4
    Burke TJ, Cronin JE, Duchin KL, Peterson LN, Schrier RW. Ischemia and tubule obstruction during acute failure in dogs: mannitol in protection. Am J Physiol 1980; 238: F30514
  • 5
    Lytton B, Glazier WB, Chaudry IH, Baue AE. The use of adenosine triphosphate with magnesium chloride in the treatment of post ischemic renal injury. Trans Am Assoc Genitourin Surg 1978; 70: 1458
  • 6
    Rocca Rossetti S. Impact of acute ischemia on human kidney. In MarbergerM, DreikornA eds., Renal Preservation. Baltimore-London: William & Wilkins, 1983: 2137
  • 7
    Stackl W, Hofmann E, Marberger M. Is the solitary kidney a privileged kidney? Br J Urol 1983; 55: 4604
  • 8
    McDougal WS. Renal perfusion/reperfusion injuries. J Urol 1988; 140: 132530
  • 9
    De Maeyer P, Oosterlink W, De Sy W. Prevention of vasospams during extensive renal surgery. An experimental study in rats. Eur Urol 1981; 7: 2246
  • 10
    Fitzpatrick JM, Monson JR, Gunter PA, Watkinson LE, Wickham JE. Renal accumulation of ammonia: the cause of post-ischaemic functional loss and the ‘blue line’. Br J Urol 1982; 541: 60812
  • 11
    Wilson DH, Barton BB, Parry WL, Hinshaw LB. Effects of intermittent versus continuous renal arterial occlusion on hemodynamics and function of the kidney. Invest Urol 1971; 8: 50715