Reduced glomerular function in rheumatoid arthritis.

Bacteriuria in rheumatoid arthritis.

“…The majority of the twenty patients with a history of abnormally high and prolonged ingestion of analgesic mixtures investigated by Steele, Gyory, and Edwards (1969) were shown to have deficiencies in both glomerular and tubular function, and one might expect to find such abnormalities in patients with rheumatoid arthritis, since most of them will have taken anti-inflammatory-analgesic drugs, and more particularly salicylates-in large quantities over a protracted period. Although tubular function has not as yet been adequately investigated in patients with rheumatoid arthritis, studies of glomerular filtration rate (Burry, 1972) and urine culture, as in the present survey, have not shown any correlation with analgesic drug consumption. There is therefore little evidence to incriminate drug-taking habits as the cause ofrenal abnormalities, apart from an apparently increased incidence of bacteriuria in steroid-treated patients as noted in this study.…”

“…The microscopic features may be indistinguishable from those known as chronic interstitial nephritis, and are common to pyelonephritis, papillary necrosis, analgesic nephropathy, ischaemia, and sometimes uric acid nephropathy. Biopsy material (Brun, Olsen, Raaschou, and S0rensen, 1965;Pasternack, Wegelius, and Makisara, 1967;Burry, 1971) has shown a high incidence of chronic interstitial nephritis and in many of these cases bacteriuria was not present. Thus it seems unlikely that the changes referred to as pyelonephritis indicate parenchymal infection.…”

“…Patients with rheumatoid arthritis have been shown to have impaired glomerular filtration, the degree of abnormality showing correlation with the severity of disease (Sorensen, 1960;Burry, 1972), and to have an increased incidence of interstitial nephritis at post mortem. Vascular insufficiency would explain both the fall in the glomerular filtration rate and the presence of chronic interstitial nephritis in post mortem and biopsy material.…”

Urinary copper excretion in rheumatoid arthritis.

“…Although there have been suggestions in the past of an abnormal copper/caeruloplasmin ratio in rheumatoid arthritis, we have been unable to confirm this. Second, since impaired glomerular function and proteinuria are relatively common in rheumatoid disease (Bulger, Healey, and Polinsky, 1968;S0rensen, 1960;Burry, 1972), the possibility must be considered that the 'excess' copper in urine depends on abnormal caeruloplasmin excretion. This explanation too is contradicted by our preliminary studies which suggest that little if any urinary copper in these patients is caeruloplasmin-bound.…”

The Kidney and Arthritis

“…Renal failure is a common cause of death in patients suffering from rheumatoid arthritis (Duthie et al 1964) and significant renal lesions have been noted in 72 % of patients with rheumatoid arthritis coming to post-mortem (Lawson & Maclean 1966). The GFR has been seen to be reduced in patients with rheumatoid arthritis when compared with a control population (Richter 1942, Heidelmann et al 1956, Sorensen 1964, Bulger et al 1968, Burry 1972) and there is evidence to suggest that at least in some cases the renal impairment is a result ofrheumatoid disease itself (Sorensen 1964, Burry 1972). Nevertheless many of the drugs used in the treatment of this complaint are associated with well-defined renal disease.…”