that the decline in percentage of renal function of the injured renal unit correlated to the severity of renal injury, with 44.7 ± 8.4% residual function for grade II–III injuries, 41.8 ± 9.2% residual function for grade IV injury, and 29.5 ± 7.9% residual function for grade V injuries [104]. Notably, all patients had normal serum creatinine at follow‐up. This group re‐assessed renal function for a subset of these patients at one year post‐injury, finding that renal function remained stable over this time period [105]. These results are supported by another study of 67 renal injuries (36% blunt trauma) that underwent post‐injury dimercapto‐succinic acid renal scan and found that the mean decrease in renal function corresponded to injury grade (p < 0.005 in multivariate analysis), with a mean decrease in renal function of 15% for grade III, 30% for grade IV, and 65% for grade V injuries [106]. In multivariate analysis, there was no difference in the decrease in renal function between blunt and penetrating renal injury or in those injuries that were managed operatively versus conservatively.
A study evaluating 52 patients who underwent renal reconstruction after renal trauma found that renal function on the reconstructed side had a mean 39.3% preservation of function, with 81% of patients having more than one‐third function of the injured kidney based on radionucleotide scintigraphy [107].
Two studies evaluated the rates of chronic kidney disease after renal trauma. One compared trauma patients with and without renal injuries, finding that 230 patients without renal injury had an incidence of acute kidney injury of 17.4% compared to 11.4% in the patients with renal injury [108]. Another multi‐institutional study evaluating grade IV and V renal injuries (49% blunt trauma) found that 6/89 patients developed chronic kidney disease (CKD) (serum creatinine range 2.0–15.6 mg/dl), and of these 6 patients, 3/5 with long‐term follow‐up developed progressive and permanent renal failure requiring dialysis [80].
Hypertension
Patients who sustain renal injuries have an increased risk of renovascular hypertension, with the incidence of renal trauma‐related hypertension estimated between less than 1 and 5% [80109–113]. As a result, the European Association of Urology (EAU) Guidelines on Urologic Trauma, the AUA Urotrauma Guidelines, and the Societé Internationale d'Urologie (SIU)/World Health Organization (WHO) consensus statement on renal trauma all recommend periodic monitoring of blood pressure for the first year after injury, at least for a subset patients who have sustained high‐grade injuries [30, 37, 82].
Renovascular hypertension after trauma may develop through several mechanisms: renal arterial stenosis or occlusion, parenchymal compression caused by perinephric hematoma (Page kidney), or chronic scar formation [109, 111, 112]. All of these result in a reduction in renal blood flow, which can then cause a unilateral hypersecretion of renin and resultant hypertension [25]. Diagnosis can be made with selective angiography and renal vein renin levels. Older studies of renal trauma patients show rates of new‐onset hypertension of 4–5%, with onset between two weeks and eight months of injury [80, 112]. A more recent study contradicts these data, showing that patients who develop hypertension after renal trauma typically manifest it during their initial hospitalization and do not develop delayed hypertension during long‐term follow‐up [114].
Management with medications, renal artery bypass surgery, or partial or total nephrectomy has been shown to be effective [109, 111]. In studies evaluating conservative treatment, treatment rates range from 28 to 50% [111, 112, 114, 115]. In terms of surgical management, elevated renin levels from the affected kidney have been shown to predict a good response to surgical treatment [111, 116]. Similarly, one study showed that in cases of arterial stenosis or occlusion, early nephrectomy within the first year after injury had better response rates compared to delayed nephrectomy [108].
Other Complications
Other rare complications may include chronic pyelonephritis, post‐trauma hydronephrosis, stone formation, fistulae, or flank pain [82].
Mortality
Mortality following renal trauma is nearly always related to associated injuries, with estimates of renal trauma driven mortality at less than 0.1% of all deaths [25].
Conclusions
The majority of renal trauma is caused by blunt mechanisms, making it vital for emergency providers and surgeons to have an understanding of renal trauma. Evaluation and management of blunt renal trauma has evolved significantly over the past decade. Guidelines from urologic societies have helped to disseminate indications for imaging and managing high‐grade kidney injuries. Over time, there has been an evolution toward non‐operative management, as data have shown good success with conservative approaches. The goal of diagnosing and managing renal trauma should be to preserve renal function, and this includes appropriate treatment of complications and failed conservative management. Long‐term follow‐up and assessment of renal function in these patients is lacking and requires updating.
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