Complete post-operative resolution of "temporary" end-stage kidney disease secondary to aortic dissection without static renal artery obstruction: a case study.

BACKGROUND: Acute kidney injury (AKI), which may progress to end-stage kidney disease (ESKD), is a potential complication of aortic dissection. Notably, in all reported ESKD cases secondary to aortic dissection, imaging evidence of static obstruction of the renal arteries always shows either renal artery stenosis or extension of the dissection into the renal arteries. CASE PRESENTATION: We present the case of a 58-year-old man with hypertension who was diagnosed with a Stanford type B aortic dissection and treated with medications alone because there were no obvious findings indicative of dissection involving the renal arteries. He had AKI, which unexpectedly progressed to ESKD, without any radiological evidence of direct involvement of the renal arteries. Thus, we failed to attribute the ESKD to the dissection and hesitated to perform any surgical intervention. Nevertheless, the patient's hormonal levels, fractional excretion values, ankle brachial indices, and Doppler resistive indices seemed to indirectly suggest kidney malperfusion and implied renal artery hypo-perfusion. However, abdominal computed tomography imaging only revealed progressive thrombotic obstruction of the false lumen and compression of the true lumen in the descending thoracic aorta, despite the absence of anatomical blockage of renal artery perfusion. Later, signs of peripheral malperfusion, such as intermittent claudication, necessitated surgical intervention; a graft replacement of the aorta was performed. Post-operatively, the patient completely recovered after 3 months of haemodialysis, and the markers that had pre-operatively suggested decreased renal bloodstream normalised with recovery of kidney function. CONCLUSIONS: To the best of our knowledge, this is the first report of severe AKI, secondary to aortic dissection, without direct renal artery obstruction, which progressed to "temporary" ESKD and was resolved following surgery. This case suggests that only coarctation above the renal artery branches following an aortic dissection can progress AKI to ESKD, despite the absence of radiological evidence confirming an obvious anatomical blockage. Further, indirect markers suggestive of decreased renal blood flow, such as ankle brachial indices, renal artery resistive indices, urinary excretion fractions, and hormonal changes, are useful for evaluating concomitant AKI and may indicate the need for surgical intervention after a Stanford type B aortic dissection.

Effects of pharmacist participation in chronic kidney disease (CKD) network and CKD manual distribution on drug-related kidney injury.

PURPOSE: Renin-angiotensin system (RAS) inhibitors carry a risk of normotensive ischemic acute kidney injury in dehydration and concurrent nonsteroidal anti-inflammatory drug (NSAID) use. Although the estimated number of patients with chronic kidney disease (CKD) is 20 000, Fujieda, Japan, has only three nephrologists. On 25 March 2016, we reorganized the CKD network to include pharmacists and distributed a CKD manual. We assessed effects of pharmacist participation in the CKD network and CKD manual distribution on patient hospitalizations because of drug-related kidney injury. METHODS: Changes in the prevalence of RAS inhibitor-related estimated glomerular filtration rate (eGFR) declines of greater than or equal to 30% and hyperkalemia of greater than or equal to 6.0 mEq/L in 129 hospitalized CKD patients, drug prescriptions of 14 150 hospitalized patients, and annual medical checkup data in 36 042 citizens were investigated before and after pharmacist participation. RESULTS: After pharmacist participation, patient hospitalizations due to RAS inhibitor-related eGFR declines decreased (71.4% to 38.1%, P = .03) and hyperkalemia declined (38.1% to 9.5%, P = .03). Pharmacist participation influenced the decrease in RAS inhibitor-related eGFR declines (P = .03). NSAID prescriptions decreased (13.4% to 11.8%, P = .003) and acetaminophen prescriptions increased (6.6% to 8.0%, P = .002) among 14 150 hospitalized patients, whereas RAS inhibitor prescriptions decreased (43.2% to 39.4%, P = .002) among 6930 hospitalized patients with eGFR less than 60 mL/min/1.73 m2 . A significant number of citizens shifted from CKD stage G3a-3b to G1-2. CONCLUSIONS: Pharmacist participation in the CKD network and CKD manual distribution decreased both hospitalizations due to RAS inhibitor-related kidney injury and citizens with CKD stage G3a-3b.