Laudable pus - lardaceous kidneys.

Amyloidosis frequently affects the kidney leading to proteinuria and loss of function. In cases of AA (reactive/inflammatory) amyloidosis, it is sometimes possible to quench the stimulus to chronic inflammation and by so doing stop further elaboration and deposition of amyloid fibrils. We describe the case of a man with a long-standing empyema who developed nephrotic syndrome and renal impairment. The empyema was resected and shortly afterwards proteinuria disappeared and renal function improved. Strenuous efforts are mandatory to locate and definitively treat underlying inflammatory foci in AA amyloidosis.

A late complication of spousal kidney donation.

An 83-year-old female who had previously (32 years ago) donated a kidney to her husband presented with loin pain, confusion and oliguria. Acute renal failure and pulmonary edema necessitated emergency hemodialysis. The history and findings were thought to be consistent with acute renal artery occlusion on a background of atherosclerosis and severe renal artery stenosis. We present this case, not to imply that renal donation is a hazardous procedure, but rather as an illustration of a complication of donor nephrectomy that in a very large series has proved to be extremely rare. This case illustrates the point that even very rare events become more likely as the period of follow-up increases.

Nephrotic syndrome: more than just oedema.

Oedema is the commonest presenting symptom and sign in nephrotic syndrome. Hypercholesterolaemia, thromboembolic events, and infectious complications may also be features. Three patients are described, each of whose nephrotic syndrome presented with a less common symptom or sign--recurrent pleural effusion, hypercholesterolaemia and oedema, pulmonary embolism--and, as a result, experienced some diagnostic delay. By forgetting to consider nephrotic syndrome, and its underlying causes, there may be inappropriate investigations and treatment for the patient.

Effect of chronic renal failure on mortality rate following arterial reconstruction.

BACKGROUND: There is some evidence that patients with renal failure who have arterial procedures may have a poor outcome. This study compared the hospital mortality rate of arterial surgery in patients with chronic renal failure and those with normal renal function. METHODS: A consecutive series of 1718 patients undergoing arterial reconstructive surgery (excluding amputation) was entered prospectively on to a computerized database. Chronic renal failure was defined as a serum creatinine level over 400 micromol/l, or dialysis (either peritoneal or haemodialysis), or a successful renal transplant. Mortality was assessed at 30 days or in hospital. RESULTS: There were 69 patients (4.0 per cent) who were defined as having chronic renal failure. The mortality rate in this group was 23 per cent (16 patients) compared with 7.3 per cent (120 patients) of the 1649 patients without renal failure. The mortality rate was highest in patients undergoing urgent or emergency surgery and in those undergoing reconstruction for lower limb occlusive disease. The main causes of death were related to the cardiovascular system. CONCLUSION: Patients with chronic renal failure undergoing arterial surgery have a poor outcome compared with those with normal renal function.

Renovascular disease.

The gold standard for the diagnosis of renal artery stenosis is angiography, with response to treatment the proof of its significance. Non-invasive methods of investigation are required and are now available including functional imaging, ultrasound, CT and MR angiography and the merits and limitations of these tests are discussed.

Individual kidney function in atherosclerotic nephropathy is not related to the presence of renal artery stenosis.

BACKGROUND: Atherosclerotic renovascular disease is increasingly recognized as an important cause of renal failure in patients over 60 years of age but the processes leading to renal dysfunction have not been defined. We have examined the relationship between renal artery stenosis and individual renal function in patients with atherosclerotic renal artery stenosis. METHODS: In this prospective descriptive study over a 25-month period, we examined the relationship between the presence of renal artery stenosis and single kidney glomerular filtration rate (SKGFR). SKGFR was measured using a novel method of synchronous (51)Chromium ethylenediamine tetraacetic acid glomerular filtration rate ((51)CrEDTA-GFR) and (99m)Technetium dimercaptosuccinic acid ((99m)TcDMSA) scintigraphy. We studied 79 patients with a mean age of 68.9 years (25.2-88.2), 44 males and 35 females. The mean age of the males was 70 years (60-80) and females 67 years (25.2-88.2). RESULTS: We found that the precision of the SKGFR was 2 ml/min. For paired kidneys we found: (i) no significant difference between kidneys with stenosis (17.3 ml/min) compared to those without stenosis (13.6 ml/min) (P=0.22); (ii) kidneys with occluded renal arteries had significantly less function (2.6 ml/min) than those without occlusion (24.5 ml/min) (P<0.05). When degree of renal arteries stenosis was correlated with SKGFR there was a reduction with an increasing degree of stenosis (<30% 27 ml/min, 30-60% 17.7 ml/min, >60% stenosis 15 ml/min, P=0. 016). CONCLUSIONS: These data demonstrate that SKGFR provides a reproducible measure of individual kidney function. There was a similar impairment of function in paired kidneys with and without renal artery stenosis, but occlusion was associated with significant reduction in function compared to the contralateral kidney. This suggests that there is a process causing renal dysfunction in patients with atherosclerotic disease independent of renal artery narrowing.

Lipid profiles in patients with atherosclerotic renal artery stenosis.

BACKGROUND: Atherosclerotic renal artery stenosis (ARAS) is an important cause of renal disease in the elderly, and these patients have a high morbidity and mortality. There are no data on their blood lipid profiles. METHODS: The lipoprotein profiles were examined in patients with proven ARAS and compared with patients matched for age, gender, renal function and presence of diabetes. RESULTS: The profiles did not show any significant difference for apolipoprotein B (control 1.31 +/- 0.39 vs. ARAS 1.24 +/- 0.28; mean +/- SD), cholesterol (control 5.65 +/- 1.28 vs. ARAS 6.12 +/- 1.29), LDL cholesterol (control 3.72 +/- 1.03 vs. ARAS 4.06 +/- 1.18), fibrinogen (control 2.48 +/- 1.39 vs. ARAS 3.29 +/- 1.49), HDL cholesterol (control 1.16 +/- 0.38 vs. ARAS 1.00 +/- 0.26) and triglyceride (control 1.68 +/- 0.80 vs. ARAS 2.32 +/- 1.73) levels between the groups. Surprisingly lipoprotein(a) levels were higher in the control group (0.58 +/- 0.45) vs. ARAS (0.31 +/- 0.21). The most striking abnormality was the markedly lower apolipoprotein A1 levels in the ARAS group (control 2.09 +/- 0.55 vs. ARAS 0.95 +/- 0. 30) and apolipoprotein A1/B ratio (control 1.74 +/- 0.71 vs. ARAS 0. 78 +/- 0.24). CONCLUSION: The lipoprotein abnormality in ARAS mirrors that in other severe vascular diseases. Potential therapeutic interventions in patients with ARAS should consider treatments to modify the apolipoprotein A1 concentration rather than cholesterol alone.

Atherosclerotic nephropathy.

BACKGROUND: Lipid moieties may have direct or indirect effects on the kidney. The association of aortic atherosclerosis and renal artery stenosis has focused interest on this as an important cause of end-stage renal failure. This article seeks to examine the evidence for the entity of atherosclerotic nephropathy. METHODS: Published data on the incidence of atherosclerotic renal artery stenosis as the cause of end-stage renal failure are presented, as well as the associated features of atherosclerotic renal stenosis. RESULTS: Atherosclerotic renal artery stenosis (ARAS) has been estimated to be the cause of between 14 and 25% of patients reaching end-stage renal failure in older age groups. There is considerable evidence of proteinuria in patients with ARAS. Recent data have shown that renal length may decrease by 1 cm or more in 35% of kidneys with > 60% stenosis. However, other data suggest that renal function in kidneys without renal artery stenosis but with contralateral renal artery stenosis may be similarly decreased. CONCLUSION: Many processes contribute to renal dysfunction in atherosclerotic aortic disease. Although ischemia may play a role, there is considerable evidence that processes such as atheroembolic disease may be important, and it would be better to use the term "atherosclerotic nephropathy" for this important disease entity.

Proteinuria in atherosclerotic renovascular disease.

Proteinuria is well described in atherosclerotic renovascular disease (ARVD), but the prevalence is unknown, and the pathogenesis may vary between patients. Substantial proteinuria (> 2 g/day) however, would be regarded by many as atypical of ARVD. We studied 94 patients (52 male) with ARVD, median age 67 years (range 49-87). Digital subtraction angiography was performed on all patients. Protein was assayed in 24-h urine samples and GFR derived using the Cockroft-Gault formula. Forty-nine patients (52%) had proteinuria < 0.5 g/24 h. Proteinuria increased with worsening renal function. Biopsies from seven non-diabetic patients with substantial proteinuria showed: minimal changes (1); glomerular sclerosis with marked ischaemic changes (3); focal glomerulosclerosis (2); and athero-emboli (1). Proteinuria, rather than being indicative of other pathology, is often a marker of severity of parenchymal disorder in atherosclerotic nephropathy, which itself is the major determinant of renal dysfunction in patients with ARVD.