An unusual case of acute on chronic renal failure following percutaneous coronary intervention

Abstract

Contrast nephrotoxicity is a common and well-documented complication of procedures utilising x ray contrast medium. It should be looked for whenever patients are exposed to contrast medium as it carries a good prognosis if managed appropriately, with only a minority of cases requiring dialysis. It is essential, however, that other causes of renal dysfunction are excluded before making a firm diagnosis of contrast nephropathy. Any delay in administering the appropriate treatment depending on the underlying pathology can result in devastating consequences. The differential diagnosis of acute renal failure is extensive and a systematic diagnostic approach should always be observed.

BACKGROUND

Percutaneous coronary angiography and intervention is an increasingly used tool in the field of cardiology. Rates of coronary angiography are increasing annually in the UK as the recent advances in the techniques and equipment used make percutaneous coronary intervention a relatively safe, minimally invasive and efficient method of coronary re-perfusion.¹ One of the common complications encountered is contrast-induced nephropathy, with an incidence of up to 2% in the general population. The incidence, however, increases significantly with the presence of risk factors and has been reported to vary from 12% up to 50% in some series.^2,3 It is defined as a relative increase of serum creatinine by 25% or an absolute increase by 44 μmol/l in the absence of any other identifiable cause.

CASE PRESENTATION

A 68-year-old lady presented in our emergency department complaining of acute shortness of breath. She had a background of hypertension, hypercholesterolaemia, smoking and chronic back pain. On admission she was on atorvastatin, enalapril, lansoprazole and ibuprofen. Following a preliminary assessment she had clinical and radiological evidence of pulmonary oedema and her ECG showed evidence of ischaemia with ST depression and T wave inversion in leads AVL and V1–4. The troponin T level was found to be elevated at 0.42 μg/l, and thus the patient was treated for non ST elevation myocardial infarction by using a glycoprotein IIb/IIIa inhibitor (tirofiban), aspirin, clopidogrel and enoxaparin, and later metoprolol. The patient also received frusemide and an increased dose of ACE inhibitor.

The initial biochemistry of the patient was as follows: sodium 145 mmol/l, potassium 3.1 mmol/l, urea 10 mmol/l, and creatinine 179 μmol/l.

The patient made a good recovery and on day 5 she underwent a coronary angiogram and intervention to the right coronary artery. The pre-study renal function was as follows: sodium 137 mmol/l, potassium 3.3 mmol/l, urea 15.3 mmol/l, and creatinine 281 μmol/l.

Following the procedure the patient had an acute and dramatic deterioration of her renal function. She became oliguric and her creatinine level reached 423 μmol/l in the next 5 days. Following review by the renal team the initial impression was that of contrast-induced nephropathy. The ACE inhibitor was stopped, the dose of frusemide was decreased, and the patient was hydrated intravenously. Despite the above management her renal function continued to deteriorate rapidly with her clinical condition worsening dramatically; she developed marked fluid overload, pulmonary oedema, respiratory failure and acidosis. At that stage an ultrasound was requested, and this showed bilateral hydronephrosis. It became clear that there was underlying obstructive nephropathy of undetermined aetiology. It is of note that her erythrocyte sedimentation rate (ESR) was found to be markedly elevated at 114 mm/h.

The patient’s creatinine level reached 537 μmol/l when bilateral nephrostomies were inserted on day 12. The recovery of renal function was immediate and dramatic, with the creatinine level near normal in the next 3 days.

On day 16 the patient had a nephrostogram which revealed right-sided obstruction at the level of the iliac crest and on the left at L4/5. The features were suggestive of extrinsic compression within the retroperitoneum (fig 1).

Figure 1.

Nephrostogram demonstrating bilateral dilatation of the collecting system with clubbed calyces and bilateral ureteric obstruction.

On day 19, the patient had a CT scan of the abdomen (fig 2), and this demonstrated mild residual hydronephrosis and a soft tissue mass/fibrosis around the abdominal aorta which was partly compressing the inferior vena cava and causing bilateral ureteric occlusion. The findings were consistent with retroperitoneal fibrosis. The patient was then commenced on high-dose oral steroids (prednisolone 60 mg daily) with significant improvement of the ESR within days. On day 26, the nephrostomies were clamped with no effect on the urine output or her renal indices, and thus they were removed on day 27. The patient was discharged on day 28 with a creatinine level of 110 μmol/l and followed up with no further deterioration in her renal function.

Figure 2.

Abdominal CT at the level of the second lumbar vertebra. There is residual hydronephrosis and a clearly visible soft tissue mass surrounding the aorta. The inferior vena cava is partly compressed.

DISCUSSION

Retroperitoneal fibrosis (RPF) appears as a mass of white, fibrous tissue that covers the retroperitoneum. Structures including the aorta, vena cava, the ureters and the psoas muscle can be embedded in this dense fibrous mass. This can result in a variety of clinical manifestations depending on the structure being compressed: obstructive uropathy and renal failure, claudication, leg oedema, hypertension and occasionally bowel obstruction.

It is a relatively rare condition with an incidence of 1 in 200 000 of population and age of predominance between the fourth and sixth decade.^4,5 The great majority of the cases are idiopathic (about 68%), though it is believed to be associated with an autoimmune response to ceroid, which is an insoluble lipid leaking through a thinned arterial wall from atheromatous plagues. Other recognised associations include the presence of abdominal aneurysm, the use of certain drugs (methysergide, β blockers and methyldopa), infection, radiation, chemotherapy and malignancy.

Common laboratory investigations frequently reveal normochromic, normocytic anaemia, markedly elevated ESR, uraemia, increased white cell count and pyouria. Helpful imaging modalities include ultrasound scanning (hydronephrosis/hydro-ureters), intravenous pyelogram (dilated collecting system, level of obstruction) and CT/MRI scanning, which is the preferred diagnostic examination and can provide superior delineation of the extent of the mass. Plain radiography can only provide non-specific findings related to the late complications of fibrosis.

The management of RPF is centred on relieving the obstruction in the acute phase, and controlling the disease process in the long run. The interventions commonly used for relieving the obstruction include percutaneous nephrostomy, retrograde stenting (JJ stent) and surgical ureterolysis. The disease process can be controlled with steroids and other immunosuppressive drugs⁶ such as azathioprine and cyclophosphamide. There have also been reports of control of the disease with tamoxifen.⁷ Where RPF is secondary to an underlying cause this should be removed or corrected.

In this case there was no obvious underlying cause for the fibrosis. The immediate improvement was a result of the relief of the mechanical obstruction following the insertion of bilateral nephrostomies. The disease process however responded well to high-dose steroids, as suggested by the low creatinine levels even following removal of the nephrostomies.

It is evident that there was a series of insults to the renal function eventually leading to fulminant renal failure. In the presence of undiagnosed obstructive nephropathy the combination of nephrotoxic therapy such as diuretics and escalation of ACE inhibition and eventually the exposure to contrast medium provoked a catastrophic deterioration of the renal function. The steady rise of creatinine levels from admission to the pre-procedure levels is suggestive of pharmacologically induced pre-renal failure through acute tubular necrosis even before the exposure to the contrast medium, which had a dramatic effect on the renal function. The exact mechanism of contrast nephrotoxicity is not entirely understood but the mechanism most likely responsible is contrast-induced renal tubular ischaemia by altering renal haemodynamics: Exposure to radiocontrast initially induces a short-lived increase in renal blood flow, and this is is followed by a prolonged phase of renal artery vasoconstriction and decreased renal perfusion.⁸ Moreover this effect is further exacerbated by the increased metabolic demand posed on the renal tubules that actively secrete contrast from the circulation. As a result, the kidneys face a combination of decreased renal perfusion and increased metabolic demand.

There is also increasing evidence to suggest that reactive oxygen species have a role in the mechanism of contrast nephrotoxicity,^9,10 causing direct tubular epithelial cell toxicity and adding to the tubular ischaemia described above.

Our experience in this case demonstrates the importance of close follow-up of patients with significant risk factors who have been exposed to x ray contrast agents. It is essential that these patients are identified promptly and offered the appropriate preprocedure and postprocedure management aiming to minimise the nephrotoxic effects of such agents. Specifically in cases of significant pre-existing renal impairment a systematic diagnostic approach is of vital importance for reaching the correct diagnosis early and avoiding diagnostic confusion. We recommend that departments routinely using intravenous contrast agents follow a standard protocol to stratify patients according to their risk of developing contrast nephropathy and implementing the appropriate management strategy.

LEARNING POINTS

• Early identification, follow-up and management of patients at risk of contrast nephrotoxicity are crucial.

• All patients with acute renal failure should be investigated thoroughly for the underlying cause.

• Be aware and vigilant of rare pathologies even in “obvious” cases.