7b TUBULOINTERSTITIAL DISEASES Year 4 Internal Medicine Notes

7b TUBULOINTERSTITIAL DISEASES Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / IMED 4.2 / Mogere -- Slide 1 TUBULOINTERSTITIAL DISEASES Dr Alex Mogere Consultant physician Slide 2 Outline Introduction AIN(Acute interstitial nephritis) CIN(Chronic interstitial nephritis) Reflux nephropathy Renal papillary necrosis Sickle cell nephropathy Cystic kidney diseases Slide 3 Introduction Affect the renal tubules and interstitial components of the renal parenchyma X-terized by: tubular dysfunction with electrolyte abnormalities,\nmoderate levels of proteinuria and\nvarying degrees of renal impairment Slide 4 Collecting duct system Slide 6 Causes of AIN Drugs: Penicillins, Nsaids, thiazides, furosemide,PPIs, indinavir,ciprofloxacin, cephalosporins, beta lactams,rifampin,mesalazine,and others(2/3 of cases) Autoimmune disorders/other systemic diseases: SLE, sjogrens, sarcoidosis Infections: legionella, leptospirosis, streptococcal orgs, TB, hantavirus, EBV, E coli (10-15% of cases) Systemic conditions- 10-15 % of cases Idioapthic -5-10% of cases Tubulointerstitial nephritis with uveitis(TINU) syndrome n/b- 10-20 % of all AKIs are due to AIN Slide 7 Clinical presentation AIN acute or subacute onset of nausea, vomiting, and malaise Typically there is renal impairment\nDrug hypersensitivity rxns- fver, rash, eosinophilia Modest proteinuria Urinalysis-rbcs, wbcs, sterile Mostly non oliguric AKI Occassionally rapid renal impairment(like in RPGN) 96 percent of patients with IgG4-related AIN have extrarenal lesions- sialadenitis, LN+, dacryoadenitis Slide 8 Invxs AIN Renal biopsy: intense inflammation, with infiltration of the tubules and interstitium by polymorphonuclear leucocytes, monocytes,and T lymphocytes. +/- eosinophils(esp in drug induced) Rfts- raised creat X-tersistic urine sediment-usu reveals wbcs, rbcs, and white cell cast Proteinuria High fractional Na excretion Slide 9 Mx AIN Drug withdrawal(drug induced AIN) high-dose corticosteroids (prednisolone 1 mg/kg/day) +/- Dialysis(usu short term) Tx primary cause if possible n/b-DDX –other causes of AKI Slide 10 Chronic interstitial nephritis(CIN) X-terized by: renal dysfunction with fibrosis infiltration of the renal parenchyma by lymphocytes, plasma cells and macrophages, tubular damage. Slide 11 Causes of CIN Slide 12 Clinical presentation CIN Most in adult life with CKD(stage 3), hypertension and small kidneys.\nelectrolyte abnormalities are typically more severe, resulting in hyperkalaemia and acidosis(tubular unresponsiveness) Urinalysis- non specific +/- salt-losing nephropathy(typical), x-terized by hypotension, polyuria and features of Na and H2O depletion. loss of urine-concentrating ability and Na+ conservation RTA (esp in sjogrens, sarcoidosis, MM,) Acidification defects- non-anion gap metabolic acidosis Slide 13 Ct. Clinical presentation CIN +/- proteinuria- < 1gm/d Anemia- early in the course secondary to destruction of erythropoeitin (EPO) producing interstitial cells Painless hematuria, Cortical scarring Renal papillary necrosis Slide 14 Mx of CIN Correction of acidosis and hyperkalaemia;\nReplacement of fluid and electrolytes (usu hypotonic fluids) RRT if irreversible renal damage has occurred. Na+ cont. fluids may cause Na+ retention and edema Often have a blunted response to loop diuretics Slide 15 Reflux nephropathy (chronic pyelonephritis) Associated with: Vesicoureteric reflux (VUR) in early life\nThe appearance of scars in the kidney Pathology: patchy interstitial scarring, tubular atrophy, and loss of nephron mass.\nRN can be acquired or congenital due to chronic reflux of urine from the bladder into the ureters + recurrent UTI in childhood renal scars can occur, even in the absence of infection.\nefforts to correct VUR by using surgical or other means are ineffective in halting progression of the disease Slide 16 Risk factors for RN The severity of VUR Recurrent UTI Bladder-bowel dysfunction. Younger age Delay in the treatment of UTI Slide 17 Clinical presentation Reflux nephropathy renal scarring and dilatation are asymptomatic\nHtn(any age) Proteinuria CKD frequency of micturition, dysuria and lumbar pain. VUR may occur in children but diminishes as the child grows, Urinalysis- leucocytes and moderate proteinuria (usually < l g/24 hrs) Increased risk of renal stone formation Htn/proteinuria in pg Prolonged child UTIs Asymptomatic bacteriuria in pg Slide 18 Ct. Clinical presentation reflux nephropathy Children and adults with small or unilateral renal scars have a good prognosis, provided renal growth is normal With significant unilateral scars there is usually compensatory hypertrophy of the contralateral kidney. Slide 19 Invxs/Reflux nephropathy Basic metabolic panel (BMP) or comprehensive metabolic panel (CMP) Urinalysis Complete blood count Urine protein to creatinine ratio Slide 20 Ct.Invxs /reflux nephropathy U/S-poor sensitivity,only capable of detecting mjr defects and excluding significant obstruction. Radionuclid