NEPHRITIS

Tubulointerstitial Nephritis (TIN)

Ms. Harpreet Kaur Lecturer

DEFINITION
Nephritis suggests a noninfectious inflammatory process that involves the nephron . Term nephritis is also applied to a group of unrelated inflammatory disorders known collectively as tubulointerstitial nephritis (TIN) . TIN initially affects mainly the interstitium and renal tubules Nephritis is term used to clinically denote a child with hypertension, decreased renal function, hematuria, and edema.

ETIOLOGY
Antigen-antibody complexes trapped in the renal parenchyma : process of inflammation and cell proliferation, in which endothelial or epithelial cells are stimulated to proliferate in varying degrees, is initiated, which damages normal renal tissue An infection, a drug, a metabolic abnormality

EPIDEMIOLOGY
TIN is very rare in children younger than age 5 years. Acute TIN can potentially occur in people of any age. Chronic TIN tends to occur late in childhood or adolescence

CLINICAL MANIFESTATIONS
Allergic manifestations, most have fever Nonspecific symptoms, such as malaise, fever, anorexia, or weakness, may be present Facial swelling and perioral, or pedal edema or ascites Symptoms of pulmonary edema or congestive heart failure (eg, dyspnea with exertion, orthopnea, shortness of breath) may be present

CLINICAL MANIFESTATIONS
Gross hematuria (eg, dark, rust colored, coke colored, tea colored) may be present. With severe hypertension, identify nosebleed, headache, or encephalopathy.

DIAGNOSTIC EVALUATION
PHYSICAL EXAMINATION Elevated blood pressure is an important physical finding Look for edema The child may have a pale appearance Tachypnea, dyspnea, hepatic congestion, and gallop rhythm suggest fluid overload with congestive heart failure

DIAGNOSTIC EVALUATION CONTD..

With tubulointerstitial nephritis (TIN), physical findings include maculopapular rash, joint pain (with flexion and extension), and fever LABORATORY STUDIES Electrolyte, creatinine, and blood urea nitrogen (BUN) levels Complete blood count (CBC) Urinalysis Urine culture

DIAGNOSTIC EVALUATION CONTD..

Lupus serologies Measurement of complement components (ie, C3, C4) Antistreptolysin-O (ASO) titer Anti-DNAase B Perinuclear antineutrophil cytoplasmic antibody (PANCA) measurement Cellular antineutrophil cytoplasmic antibody (CANCA) assessment

DIAGANOSTIC EVALUATION CONTD..

Serum IgA measurement Laboratory findings in tubulointerstitial nephritis (TIN) include hematuria, eosinophilia, sterile pyuria, low-grade proteinuria, eosinophiluria, and urinary white blood cell casts

DIAGANOSTIC EVALUATION CONTD..

IMAGING STUDIES Renal ultrasonography is usually performed to exclude other causes of hypertension and hematuria, such as renal artery stenosis (ie, small, abnormal kidney on one side) No imaging tests are sensitive or specific for TIN. Renal ultrasonography may show large kidney

TREATMENT
INPATIENT CARE Inpatient care is usually necessary only to manage severe hypertension or complications of acute or chronic renal failure (eg, dialysis access, uremic syndrome, congestive heart failure, electrolyte abnormalities such as hyperkalemia and pericardial effusion)

TREATMENT
OUTPATIENT CARE Involve the use of antihypertensive, diuretics, and diet modification Outpatient therapy may involve dialysis in a child who develops end-stage renal disease

TREATMENT
DIET AND ACTIVITY Fluid restriction may prevent fluid overload Fluid restriction of 300 mL/m2/d plus losses may allow In patients with hypertension, sodium restriction to the recommended daily allowance (RDA) of 2-4 mEq/kg/d may aid in management In children with renal failure, potassium restriction is justified to prevent hyperkalemia A short-term high-carbohydrate diet may prevent catabolism of body protein as an energy source Calcium supplementation is useful to maintain normal serum calcium

MEDICAL MANAGEMENT
Diuretic agents Furosemide is a loop diuretic. It is often effective in removing fluid even when the glomerular filtration rate is reduced secondary to nephritis Hydrochlorothiazide (HCTZ) acts on the distal nephron to impair sodium reabsorption, enhancing sodium excretion

MEDICAL MANAGEMENT
ACE Inhibitors Captopril, a competitive ACE inhibitor, prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, increasing levels of plasma renin and reducing aldosterone secretion A competitive ACE inhibitor, enalapril reduces angiotensin II levels, decreasing aldosterone secretion. The drug lowers systemic arterial blood pressure, reducing injury caused by elevated blood pressure

MEDICAL MANAGEMENT
Angiotensin II Receptor Antagonists Losartan is a prototype ARB. It is specific for the type 1, as opposed to type 2, angiotensin receptor. It may induce more complete inhibition of the renin-angiotensin system than do ACE inhibitors Valsartan is a prodrug that directly antagonizes angiotensin II receptors. It displaces angiotensin II from the AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses

MEDICAL MANAGEMENT
Calcium Channel Blockers Calcium channel blockers, nifedipine causes peripheral arterial vasodilation by inhibiting calcium influx across vascular smooth-muscle cell membranes Beta Adrenergic Blockers Labetalol blocks alpha-1 beta 1-, and beta 2-adrenergic receptor sites, decreasing BP Propranolol has membrane-stabilizing activity and decreases automaticity of contractions. Propranolol is not suitable for emergency treatment of hypertension. Do not administer IV in hypertensive emergencies