Access to the kidney is via either the transperitoneal or retroperitoneal approach (supra 12th, 12th or subcostal) depending on the surgeon’s preference and tumor location. It is important that the side is marked when the patient is awake prior to the surgery. The surgical principles for an open procedure remain the same as for the minimally invasive techniques. The patient may be in the supine, lateral decubitus or full flank position, with a break in the table. The kidney is accessed by dividing along the white line of Toldt and mobilization of the colon. After identifying the upper ureter and gonadal vein, the hilar vessels are carefully dissected in preparation for subsequent step of clamping. Intraoperative ultrasound may help to locate the deep-seated tumors. Gerota’s fascia is then incised to expose the tumor and the surrounding renal capsule. Cooling the kidney down to 20–25 °C helps to prolong the ischemia time up to 3 h of arterial occlusion [7]. Laying ice slush around the kidney is the most common method. Other techniques include intra-arterial and intra-ureteric cooling which are not commonly used. The renal artery, which lies posterior to the vein, is clamped first before the vein using a bulldog or Satinsky clamp. After excising the tumour sharply with surrounding rim of normal renal tissue, the raw area is closed with interrupted absorbable sutures using surgicel rolls for a tamponade effect. Several clinical studies suggest that the maximum period of warm ischemia time (WIT) for preservation of renal function should not exceed 20 min [7].

Ischemic insults such as clamping often results in cellular damage of the nephron and renal vasculature due to necrosis and apoptosis, inevitably leading to renal failure. Physiological changes include a fall in glomerular filtration rate, retention of nitrogenous waste products, increase in extra cellular fluid volume, and electrolyte and acid-base homeostasis. There are three mechanisms described in relation to ischemia/perfusion injury [8]: vascular, obstructive and reperfusion injury.

There is an inflammatory response to ischemia which exacerbates impairment in blood flow caused by vasoconstriction and vascular congestion, leading to a vicious cycle [9]. This damage occurs in endothelial cells of the peritubular capillaries in the outer medulla, which are marginally oxygenated even without clamping. This is followed by congestion, decreased perfusion and appearance of adhesion molecules. Adhesion molecules and pro-inflammatory and chemotactic cytokines from ischemic cells initiate leukocyte infiltration [9]. Interaction between leukocytes and endothelial cells accentuates oedema of endothelial cells and subsequent injury. There is also possible mechanism involving the renin-angiotensin mechanism.

The ischemic insult causes cellular failure of oxidative phosphorylation and ATP depletion, leading to derangement of the sodium pump. This leads to passive diffusion of sodium and chloride resulting in cellular oedema. There is also impaired sodium absorption by injured tubular cells leading to increased levels of tubular sodium concentrations. Cellular potassium and magnesium are lost, calcium is gained; anaerobic glycolysis and acidosis occur, and lysosomal enzymes are activated. These changes result in cellular death. During reperfusion, hypoxanthine, a product of ATP degradation, is oxidized to xanthine with the formation of free radicals that cause further cellular damage [10]. There is polymerization of Tamm-Horsfall (T-H) protein due to increased intratubular sodium. T-H is normally secreted by the loop of Henle, and polymerization leads to a gel and cast formation. As a result, brush-border membranes and cells slough to obstruct tubules downstream.

Once the debris starts forming the casts, the tubular obstruction gets aggravated leading to leakage of glomerular filtrate from the tubular lumen across denuded tubular walls into capillaries and into the circulation. This effectively reduces the glomerular filtration rate (GFR).

ATP depletion also activates harmful proteases and phospholipases, which, with reperfusion, cause oxidant injury to tubular cells, the so-called reperfusion injury [8].

The exact magnitude of reperfusion injury is not clear. The insult of warm ischaemia is aggravated further by restoration of blood flow because of the inflammatory response [11]. The reperfusion injury can be mediated by several mechanisms including the generation of reactive oxygen species (ROS), cellular derangement, microvascular congestion and compression, polymorphonuclear (PMN)-mediated damage, and hypercoagulation. Reperfusion with the resulting reintroduction of molecular oxygen of constricted capillaries leads to congestion and red cell trapping. This vascular effect can reduce renal blood flow by as much as 50 % [12].

Radiofrequency ablation (RFA) assisted laparoscopic partial nephrectomy (RFA-LPN) may be the way forward to remove the tumour without warm ischemia and renal hilar clamping. In a study of 78 patients undergoing NSS, 36 patients underwent laparoscopic partial nephrectomy and 42 patients RFA-assisted robotic clampless partial nephrectomy (RF-RCPN). In the latter group, a Habib 4X RFA device was used to coagulate a margin of normal parenchyma around the tumour. There was no difference in blood loss, complication rate, postoperative bleeding, renal function and recurrence rate [13]. However long term results need to be assessed. Other centres have reported similar results [14].

Laparoscopic (LPN)/robotic-assisted PN (RAPN) vs. open partial nephrectomy (OPN): Open partial nephrectomy remains the gold standard operation for NSS because it allows the operator to have adequate exposure, easy control of hilum, cold ischemia and tactile sensation during surgery. In addition other methods of vascular control such as manual compression or renal clamping could be used during OPN. In summary, the technique of tumour excision, reconstruction of renal parenchyma and control of bleeding are standardized in OPN. As mentioned earlier, OPN is increasingly being challenged by the introduction of minimally invasive techniques but LPN is carried out only in specialized centers with laparoscopic experience. LPN offers the benefits of faster post-operative recovery and lower morbidity over the open approach with similar oncological outcomes [15]. The overall cancer specific survival rate after 7 years is estimated at 92.7 and 95.5 % for laparoscopic and open NSS, respectively [16]. The main drawback of LPN is the steep learning curve required to perform this demanding procedure with concerns of higher warm ischaemia times and blood loss [17].

Over recent years there has been growing interest in RPN to overcome the limitations of laparoscopy but yet offers all the benefits of minimally invasive surgery. The main advantages of the robotic approach lie in its ergonomics with a greater range of wristed-instrument motion and 3-D vision that enables a shorter learning curve to be established. This technique, however, is still in its infancy and whilst emerging data appears promising, the long term functional and oncological outcomes remain to be determined [18]. In a retrospective review of 164 consecutive RAPN cases White et al. identified and classified 67 that were highly complex renal masses according to R.E.N.A.L. (R-Radius; E: Location & Depth- exophytic or endophytic; N: Nearness to the renal sinus fat or collecting system; A: anterior or posterior position; L- polar or non polar location) nephrometry score (>7). They concluded that WIT, blood loss and the rate of complications increased in highly complex renal masses [19].