Drug . | Potential Nephrotoxic Manifestation . | Renal Manifestation . |
---|---|---|
5-ASA | Tubulointerstitial nephritis | • Microscopic hematuria, microalbuminuria, sterile pyuria (± eosinophiluria) • Decrease in eGFR • Very rare e.g 0.3% per annum114 |
Calcineurin inhibitors | Acute kidney injury due to tubulointerstitial damage evident as electrolyte disturbances. Chronic kidney disease due to vasoconstriction/ischaemia leads to interstitial fibrosis | • Hyperkalemia, hypomagnesemia, hyperchloremic metabolic acidosis, hyperuricemia, hyperglycemia • Microalbuminuria • Hypertension • Decrease in eGFR • Increasing risk with continuous temporal exposure, especially over 5 or more years59 |
TNF-α inhibitors | Acute kidney injury Glomerulonephritis | • Microalbuminuria/proteinuria • New onset hypertension • Decrease in eGFR • Very rare (but vigilance is prudent) |
Vedolizumab | Acute interstitial nephritis | • Dipstick hematuria, microalbuminuria, sterile pyuria (± eosinophiluria) • Decrease in eGFR • Very rare (but vigilance is prudent) |
Tofacitinib | Acute kidney injury | • Decrease in eGFR • Very rare (but vigilance is prudent) |
Filgotinib | Increased drug concentration in renal impairment so reduce dose | • Monitor eGFR looking for early evidence of loss of renal function |
Drug . | Potential Nephrotoxic Manifestation . | Renal Manifestation . |
---|---|---|
5-ASA | Tubulointerstitial nephritis | • Microscopic hematuria, microalbuminuria, sterile pyuria (± eosinophiluria) • Decrease in eGFR • Very rare e.g 0.3% per annum114 |
Calcineurin inhibitors | Acute kidney injury due to tubulointerstitial damage evident as electrolyte disturbances. Chronic kidney disease due to vasoconstriction/ischaemia leads to interstitial fibrosis | • Hyperkalemia, hypomagnesemia, hyperchloremic metabolic acidosis, hyperuricemia, hyperglycemia • Microalbuminuria • Hypertension • Decrease in eGFR • Increasing risk with continuous temporal exposure, especially over 5 or more years59 |
TNF-α inhibitors | Acute kidney injury Glomerulonephritis | • Microalbuminuria/proteinuria • New onset hypertension • Decrease in eGFR • Very rare (but vigilance is prudent) |
Vedolizumab | Acute interstitial nephritis | • Dipstick hematuria, microalbuminuria, sterile pyuria (± eosinophiluria) • Decrease in eGFR • Very rare (but vigilance is prudent) |
Tofacitinib | Acute kidney injury | • Decrease in eGFR • Very rare (but vigilance is prudent) |
Filgotinib | Increased drug concentration in renal impairment so reduce dose | • Monitor eGFR looking for early evidence of loss of renal function |
Drug . | Potential Nephrotoxic Manifestation . | Renal Manifestation . |
---|---|---|
5-ASA | Tubulointerstitial nephritis | • Microscopic hematuria, microalbuminuria, sterile pyuria (± eosinophiluria) • Decrease in eGFR • Very rare e.g 0.3% per annum114 |
Calcineurin inhibitors | Acute kidney injury due to tubulointerstitial damage evident as electrolyte disturbances. Chronic kidney disease due to vasoconstriction/ischaemia leads to interstitial fibrosis | • Hyperkalemia, hypomagnesemia, hyperchloremic metabolic acidosis, hyperuricemia, hyperglycemia • Microalbuminuria • Hypertension • Decrease in eGFR • Increasing risk with continuous temporal exposure, especially over 5 or more years59 |
TNF-α inhibitors | Acute kidney injury Glomerulonephritis | • Microalbuminuria/proteinuria • New onset hypertension • Decrease in eGFR • Very rare (but vigilance is prudent) |
Vedolizumab | Acute interstitial nephritis | • Dipstick hematuria, microalbuminuria, sterile pyuria (± eosinophiluria) • Decrease in eGFR • Very rare (but vigilance is prudent) |
Tofacitinib | Acute kidney injury | • Decrease in eGFR • Very rare (but vigilance is prudent) |
Filgotinib | Increased drug concentration in renal impairment so reduce dose | • Monitor eGFR looking for early evidence of loss of renal function |
Drug . | Potential Nephrotoxic Manifestation . | Renal Manifestation . |
---|---|---|
5-ASA | Tubulointerstitial nephritis | • Microscopic hematuria, microalbuminuria, sterile pyuria (± eosinophiluria) • Decrease in eGFR • Very rare e.g 0.3% per annum114 |
Calcineurin inhibitors | Acute kidney injury due to tubulointerstitial damage evident as electrolyte disturbances. Chronic kidney disease due to vasoconstriction/ischaemia leads to interstitial fibrosis | • Hyperkalemia, hypomagnesemia, hyperchloremic metabolic acidosis, hyperuricemia, hyperglycemia • Microalbuminuria • Hypertension • Decrease in eGFR • Increasing risk with continuous temporal exposure, especially over 5 or more years59 |
TNF-α inhibitors | Acute kidney injury Glomerulonephritis | • Microalbuminuria/proteinuria • New onset hypertension • Decrease in eGFR • Very rare (but vigilance is prudent) |
Vedolizumab | Acute interstitial nephritis | • Dipstick hematuria, microalbuminuria, sterile pyuria (± eosinophiluria) • Decrease in eGFR • Very rare (but vigilance is prudent) |
Tofacitinib | Acute kidney injury | • Decrease in eGFR • Very rare (but vigilance is prudent) |
Filgotinib | Increased drug concentration in renal impairment so reduce dose | • Monitor eGFR looking for early evidence of loss of renal function |
This PDF is available to Subscribers Only
View Article Abstract & Purchase OptionsFor full access to this pdf, sign in to an existing account, or purchase an annual subscription.