The natural course of gold nephropathy: long term study of 21 patients.

To clarify the natural course of gold nephropathy and thereby facilitate its clinical management 21 patients with rheumatoid arthritis who developed proteinuria during treatment with intramuscular sodium aurothiomalate were studied in detail throughout their renal illnesses. Renal biopsies were performed, and creatinine clearance and proteinuria were measured serially for 60 months (range 16-130 months). Ten patients developed proteinuria after six months'' treatment, 15 after 12 months, and 18 after 24 months. When treatment was stopped the proteinuria reached a median peak of 2.1 g/day (range 0.7-30.7 g/day) at two months (range 1-13 months) before resolving spontaneously, in eight patients by six months, in 13 by 12 months, and in 18 by 24 months. All patients were free of proteinuria by 39 months, the median duration being 11 months. The median first and last measurements of creatinine clearance showed no significant change (77 ml/minute and 59 ml/minute, respectively), and no patient died from or needed treatment for renal failure. HLA-B8 or DR3 alloantigens, or both, were identified in seven patients. Renal biopsy specimens showed membranous glomerulonephritis in 15 patients, a minimal change nephropathy in two, mesangial electron dense deposits in two, and no appreciable glomerular changes in two. In these 21 patients the proteinuria of gold nephropathy resolved completely when treatment was withdrawn. Renal function did not deteriorate, corticosteroids were unnecessary, and several different renal lesions were seen.     

IgA nephropathy in adults: immunohistologic findings and clinical course

Laboratory examination of specimens from 123 consecutive renal biopsies performed at Victoria General Hospital, Halifax revealed six cases of mesangial deposition, predominantly of IgA, unassociated with systemic disorders. Immunohistologic examination showed deposits of only IgA in one specimen, IgA and IgG in two and IgA, IgG and IgM in three. Glomerular deposits of C3 were seen in five of the specimens, and properdin was seen in three. Glomeruli in all the specimens showed increased matrix and increased numbers of cells in the mesangium. Electron microscopy revealed deposits in the mesangium or capillary wall in all five of the specimens so studied. All six patients had proteinuria, four had microscopic hematuria, and three had hypertension; in one patient the disease progressed to renal failure.     

Declining incidence of analgesic nephropathy in Canada.

Surveys of nephrologists in Canada indicate that the incidence of analgesic nephropathy has decreased by about 50% in less than a decade in association with the removal of phenacetin from the market and restrictions on the availability analgesic mixtures containing acetaminophen and acetylsalicylic acid. The number of patients presenting with end-stage renal disease attributed to analgesics has shown a similar drop. These decreases have occurred in spite of increased consumption of acetaminophen as a single analgesic. Analgesic nephropathy should not be expected to disappear, however, since there is evidence that the drugs still in use have the potential to cause renal damage.     

I. Recognition of the problem of analgesic nephropathy

The incidence of renal impairment secondary to the abuse of analgesic compounds now accounts for a significant proportion of patients requiring renal replacement therapy. The clinical features of 100 cases of analgesic nephropathy are described; essentially these consist of otherwise unexplained renal impairment, urinary tract symptoms, radiological changes and sterile pyuria, often associated with dyspepsia, anemia and psychiatric disturbances. The classical pathological changes consist of interstitial nephritis and progressive reduction in renal size, secondary to repeated episodes of papillary necrosis. Cessation of analgesic abuse usually arrests the deterioration in renal function, and indeed some recovery of function may occur.     

Natural course of penicillamine nephropathy: a long term study of 33 patients

To elucidate the natural course of the nephropathy associated with penicillamine and thereby facilitate its clinical management 33 patients with rheumatoid arthritis who developed proteinuria during treatment with oral penicillamine were studied in detail throughout their renal illness. Renal biopsies were performed, and creatinine clearance and proteinuria were measured serially for 74 months (range 16-148 months). Fourteen patients developed proteinuria within six months after the start of treatment and 27 within 12 months. When treatment was stopped the proteinuria reached a median peak of 4·2 g/24 h (range 0·3-15·0 g/24 h) at one month (range 0-7 months) before resolving spontaneously by six months (12 patients), 12 months (21), or 18 months (29). In all patients but one, who developed carcinoma of the renal pelvis, proteinuria resolved by 21 months and its median duration was eight months. The median first and last measurements of creatinine clearance showed no appreciable change (80 ml/min and 78 ml/min), and no patient died from or needed treatment for renal failure. The HLA-B8 or HLA-DR3 alloantigen, or both, were identified in 10 patients. Renal biopsy specimens showed membranous glomerulonephritis in 29 patients, minimal change nephropathy in two, and electron dense deposits in the mesangial regions in two.In all the patients whose nephropathy was due solely to treatment with penicillamine the proteinuria resolved completely when the drug was withdrawn; renal function did not deteriorate, and corticosteroids were unnecessary.     

The role of D-dimer in relation to the clinical course of patients with COVID-19

In recent times,systemic coagulation,fibrinolysis,and cardio-pulmonary injury has been recognized in patients with COVID-19,the clinical disease state caused by infection of the novel coronavirus,SARS-CoV-2.While originally believed to be a primary lower respiratory infection,as more cases are identified,treated,and examined,hematologic complications are being identified as a significant driver of morbidity and mortality associated with the disease.Elevated D-dimer levels(>1μg/ml)on hospital admission have been identified as being associated with increased mortality[1],and levels greater than 2μg/ml predict fatal outcomes in patients[2].Alongside these results,there is also a greater risk of thrombotic events in COVID-19 patients,with risk increasing to as high as 31%[3],and pulmonary embolism risk increases proportionately alongside this[4].Whilst understanding of the pathophysiology is incomplete,there is clearly a component of coagulative disorder in these patients.D-dimer could prove a valuable tool to identify patients who are likely to have poorer outcomes and allow for prophylactic treatment and monitoring of secondary complications(Fig.1).     

Letter: Trimethoprim-sulfamethoxazole: in vitro sensitivity of 1000 clinical isolates.

Certain “primitive” peoples such as traditional-living nomadic Eskimos have as yet been spared from the current epidemic of ischemic heart disease. A review of risk factors for underdeveloped populations suggests that environment rather than constitution is responsible. Favourable factors include the absence of overeating, a substantial level of of physical activity, only recent acquisition of the cigarette habit and absence of competitiveness. However, risk factors generally operate as in the “white” community, and where a Western lifestyle is embraced through either migration or acculturation the prevalence of ischemic heart disease rapidly increases to the levels encountered in “civilized” groups.