Chris Laing

Contrast-induced acute kidney injury following PCI.

Coronary revascularization using percutaneous coronary intervention (PCI) is one of the major treatments for patients with stable coronary artery disease, with approximately 1.5 million patients undergoing PCI in the United States and Europe every year. An important neglected complication of PCI is contrast‐induced acute kidney injury (CI‐AKI).

The utility of ADAMTS13 in differentiating TTP from other acute thrombotic microangiopathies: results from the UK TTP Registry

Thrombotic microangiopathies (TMAs) are frequently difficult to differentiate clinically, and measurement of ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) remains vital in thrombotic thrombocytopenic purpura (TTP) diagnosis. We retrospectively reviewed cases referred for ADAMTS13 testing, using UK TTP Registry screening data. Of a total 810 cases, 350 were confirmed as TTP. The 460 non‐TTP cases comprised secondary TMAs (24·57%) and haemolytic uraemic syndrome (HUS) (27·17% aHUS, 2·83% Shiga‐like toxin‐producing E. coli [STEC]‐HUS); the remainder were TMAs with no clear association, not TMAs, or had no confirmed diagnosis. ADAMTS13 levels were significantly lower in TTP than STEC‐HUS, aHUS and other TMAs. TTP patients had significantly lower platelet count (15 × 109/l; range 0–96) than aHUS (57 × 109/l; range 13–145, P < 0·0001) or STEC‐HUS (35 × 109/l; range 14–106, P < 0·0001); they also had lower creatinine levels (92 μmol/l; range 43–374) than aHUS (255 μmol/l; range 23–941, P < 0·0001) and STEC‐HUS (324 μmol/l; range 117–639, P < 0·0001). However, 12/34 (35·3%) aHUS patients had a platelet count <30 × 109/l and 26/150 (17·3%) of TTP patients had a platelet count >30 × 109/l; 23/150 (15·3%) of TTP patients had a creatinine level >150 μmol/l. This study highlights the wide variety of TMA presentations, and confirms the utility of ADAMTS13 testing in TTP diagnosis.

On the alert for outcome improvement in acute kidney injury

Acute kidney injury, a sudden reduction in kidney function, has been defi ned by a rise in serum creatinine or a fall in urine volumes. Acute kidney injury presents across diverse health-care settings and is a consequence of diverse comorbid and acute risk factors. Data is emerging about a strong and independent association between acute kidney injury and adverse outcomes, including mortality and the development of chronic kidney disease. Associated health-care costs are large and could exceed those of common cancers. Care has been shown to be suboptimum in many cases. As the profi le of this syndrome has risen, local, national, and global initiatives have mobilised. Acute kidney injury has been identifi ed as a priority in a recent strategic plan for the National Health Service (NHS) in England, The Five Year Forward View. Prompt recognition and activation of a timely clinical response have been identifi ed as key to improvement of outcomes in acute kidney injury. This has led investigators to consider whether automation of these processes might have clinical use. Acute kidney injury detection through real-time, computerised algorithmic interrogation of blood results followed by clinician notifi cation has enjoyed accelerated adoption. This approach can be viewed as a form of so-called unsolicited clinical decision support. Although such automated decision-support methods have great promise, their application in clinical practice has had mixed results. In The Lancet, F Perry Wilson and colleagues report the fi rst randomised controlled trial to examine the eff ect of such an intervention on outcomes in acute kidney injury. The investigators must be congratulated for designing and executing a high-quality study and presenting their important fi ndings clearly. In this single-masked, parallel-group, randomised controlled trial, the investigators devised a computerised algorithm to detect changes in patient serum creatinine values during stays in hospital. When such changes met criteria for acute kidney injury according to the Kidney Disease: Improving Global Outcomes (KDIGO) working group classifi cation of acute kidney injury, they were randomised either to an alert group or a usual care group. In the intervention group, clinicians and pharmacists received a text prompt to pager systems informing them that their patient had acute kidney injury. This directed the clinicians to the study website and a link to a best-practice guideline. The usual care group received no alert. In anticipation of variability in the eff ect of the intervention, the investigators stratifi ed by surgical versus medical admission, and by intensive care unit versus non-intensive care unit location. The criteria for triggering of the automated alert were rigorous and dependent on having a minimum of 2 serum creatinine values, a 1·5-fold rise from a 7-day baseline, or a 0·3 mg/dL rise from a 48-h baseline. Because clinicians were directly paged with results, this can be viewed as a high-fi delity application of the approach. To avoid socalled alert fatigue, the alert only notifi ed once for each episode of acute kidney injury. The investigators assessed the intervention’s eff ect on a composite primary endpoint of relative maximum increase in serum creatinine, dialysis, or death. 1201 patients were assigned randomly to the alert group, and 1192 to usual care, and there was no benefi t in terms of the trial’s primary endpoint (p=0·88). The intervention also resulted in no eff ect on process outcomes such as bolus fl uid therapy or drug cessation. There was an increased rate of nephrology consultations in the surgical ward subgroup of the intervention group (36 patients [12%] vs 17 patients [5%] receiving usual care; odds ratio 2·29, 95% CI 1·22–4·44), but this did not improve outcomes. There are potential processes of care in acute kidney injury that were not measured, such as urine dipstick tests, treatment of sepsis, and renal imaging, but if these processes were applied more frequently in the intervention group they do not seem to have resulted in clinical benefi t. The authors rightly point out that acute kidney injury is heterogeneous in causation and therapy is not standardised. Alerting could trigger indiscriminate interventions (such as fl uid administration) that might benefi t some patients and harm others. Wilson and colleagues’ study shows that acute kidney injury, under current sensitive defi nitions, is often self-limiting. The median relative increase in serum creatinine subsequent to randomisation was close to zero in the study population. In many cases, a transient fall in glomerular fi ltration rate will be a regulatory response to a circulatory challenge. Such For the UK National Health Service campaign ‘Think Kidneys’ see www.thinkkidneys. nhs.uk

Persistent severe polyuria after renal transplant

Polydipsia and polyuria are common symptoms in patients with diabetes insipidus (DI), which can be due to inadequate vasopressin production (cranial DI) or vasopressin insensitivity (nephrogenic DI). Clinical diagnosis of the subtypes of DI can be tricky. We present a 44-year-old man with a strong family history of DI who had been diagnosed with autosomal dominant nephrogenic DI from infancy. At the age of 40, he had progressed to end-stage renal failure. When he experienced unresolving severe polyuria after renal transplant, further investigations revealed that he was misdiagnosed and that he had a novel mutation causing autosomal dominant cranial DI.

Importance of citrate and the calcium : citrate ratio in patients with calcium renal lithiasis and severe lithogenesis.

On the other hand, future surveys should gather opinions about the role of RARP for high-risk disease, standardised evaluation of surgical complications; while addressing continence and potency status along with methods of their measurement. These topics were already addressed in the Pasadena Consensus and obtaining opinions of surgeons will further provide insight as to how surgeons adapt to the ever-changing advances in this field.

Interactive Case Report: A patient with suspected miscarriage is found to have hypertension, renal failure, and thrombocytopenia: case presentation

Four weeks ago we described the case of a 46 year old woman who presented with possible miscarriage, severe hypertension, acute renal failure, pulmonary oedema, microangiopathic haemolytic anaemia, and seizures (BMJ 2007;334:1372, doi: 10.1136/bmj.39212.564745.BE). The diagnoses we considered were malignant hypertension, intrinsic renal disease, a primary microangiopathic process—such as haemolytic uraemic syndrome or thrombotic thrombocytopenic purpura, or eclampsia with HELLP syndrome. She was started on intermittent haemodialysis, an angiotensin converting enzyme inhibitor, and plasma exchange (BMJ 2007;335:44, doi: 10.1136/bmj.39239.478495.80). A magnetic resonance imaging scan of the brain showed posterior leucoencephalopathy consistent with hypertensive encephalopathy. Her platelet count, metabolic abnormalities, and breathlessness improved and she had no further seizures. At one week she was well but remained dependent on dialysis. Bisoprolol and amlodipine were added to control her blood pressure. Renal Doppler ultrasound showed poor renal perfusion so we performed angiography to exclude renovascular disease. This showed normal renal vessels (fig 1​1),), suggesting a microangiopathic infrarenal process. Fig 1 The patients bilateral renal angiography showing normal renal vessels Renal biopsy demonstrated florid myxoid intimal thickening in interlobular arteries (fig 2​2),), widespread acute tubular damage, and glomerular ischaemic changes. There was little thrombotic change to suggest haemolytic uraemic syndrome or thrombotic thrombocytopenic purpura. These appearances are consistent with a diagnosis of malignant hypertension or scleroderma renal crisis. Fig 2 The patients renal biopsy showing florid myxoid intimal thickening in interlobular arteries (A), widespread acute tubular damage (B), and glomerular ischaemic changes (C) The table ​table summarises the other investigations and blood tests. These were negative except for a strongly positive speckled antinuclear antibody at a titre of more than 1/1000. The staining pattern was consistent with anti-RNA polymerase antibodies and this was confirmed with immunoprecipitation. The patients immunological profile and results of other investigations Anti-RNA polymerase antibodies are strongly associated with scleroderma renal crisis, and we consider this to be the diagnosis. Her hypertension may have precipitated miscarriage on this occasion, but the cause of the earlier miscarriages is less clear. Scleroderma renal crisis primarily affects young and middle aged women and presents with acute renal failure and hypertension. There may be no prior symptoms of systemic sclerosis, but the history of Raynauds offered a diagnostic clue in this patient. Other features of malignant hypertension such as encephalopathy, seizures, pulmonary oedema, and microangiopathic haemolytic anaemia may complicate this illness. Angiotensin converting enzyme inhibitors may facilitate microvascular remodelling and prevent progression of renal impairment; they are used widely in this disease. Intravenous vasodilatory therapy, usually with prostacyclin, is recommended, and dialysis may be required. The benefit of plasma exchange in secondary microangiopathy is controversial and was instituted in this case because initially we could not exclude thrombotic thrombocytopenic purpura as a primary diagnosis. The prospects for renal recovery are poor in patients who need dialysis at diagnosis. This patient is currently well on haemodialysis three times a week, although she still requires oral antihypertensives. She is currently awaiting renal transplantation.