1. Pullen, Richard L. Jr. EdD, MSN, RN, CMSRN, CNE-cl, ANEF

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Q: What's tubulointerstitial nephritis and what are the priority nursing interventions?

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A: Tubulointerstitial nephritis (TIN) is an immune-mediated inflammatory process that causes tissue damage to the kidney tubules and interstitium. Damage to the kidney tubules and interstitium leads to the creation of new antigens and activation of proinflammatory cytokines that are derived from inflammatory lymphocytes and macrophages. Damage to the glomeruli and vascular structures may occur over time, causing fibrosis and sclerosis in the kidney. Progressive fibrosis in TIN may lead to a reduction in renal function and end-stage renal disease.


TIN can be chronic or acute. Chronic TIN may be caused by drugs or toxins, such as analgesics and heavy metals; hereditary disorders such as polycystic kidney disease; immune-mediated diseases such as systemic lupus erythematosus; Sjogren syndrome and sarcoidosis; hematologic diseases, such as multiple myeloma and sickle cell anemia; infections; and obstruction from stones or tumors.


Patients with chronic TIN may be asymptomatic or present with symptoms related to underlying disease or chronic kidney disease (CKD). Patients may have mild proteinuria (<1 gm in a 24-hour urine specimen); increased serum creatinine; reduced glomerular filtration rate; microscopic hematuria; eosinophilia; eosinophiluria; sterile pyuria (white blood cells in the urine in the absence of bacteria); phosphaturia; glycosuria; hypokalemia or hyperkalemia; hyponatremia; and a reduction in red blood cells (RBCs), hemoglobin, and hematocrit reflecting anemia. Serologic studies, such as antinuclear antibodies (ANA), anti-DNA, and complement levels are usually normal unless there's an exacerbation of systemic inflammatory autoimmune disease. For example, a positive anti-DNA and low complement are highly indicative of lupus glomerulonephritis. Patients may also experience nausea, vomiting, anorexia, hypertension, fatigue, edema, shortness of breath, and pruritis resulting from elevated phosphorus levels.


A diagnosis of chronic TIN is based on the patient's signs and symptoms, lab analysis, and ultrasound of the kidneys. A renal biopsy is performed when the diagnosis is uncertain and usually shows interstitial lymphocytic infiltration with eosinophils and tubular atrophy. Treatment includes eliminating the underlying cause (for example, eliminating the offending medications and treating underlying disease processes). Corticosteroids may be prescribed. Dialysis and renal transplantation may be necessary for severe disease.


Acute TIN may occur from many of the same etiologies as chronic TIN. The most frequent cause of injury in acute TIN is drug hypersensitivity. Nonsteroidal anti-inflammatory drugs; aspirin; anticonvulsants; diuretics; antibiotics; antivirals; and anticancer drugs, such as tyrosine kinase inhibitors and immune checkpoint inhibitors, are common causes of acute TIN.


Acute TIN is most often observed in patients who are exposed to multiple medications. The classic symptoms are rash, arthralgia, and eosinophilia. Fever is a common symptom. Patients may experience low back pain or flank pain if the cause is pyelonephritis. There's generally a rapid decline in renal function. Patients may have mild proteinuria, a decline in glomerular filtration rate, eosinophilia, eosinophiluria, and hyperkalemia. Diagnostic measures and treatment are similar to chronic TIN.


When caring for a patient with confirmed or suspected TIN:


* Conduct a health history interview and head-to-toe assessment. Evaluate medication history.


* Perform a cardiopulmonary assessment. Fluid overload from chronic or acute kidney disease may result in abnormal lung sounds and an increase in cardiac workload.


* Evaluate lung sounds, respiratory rate and depth, and oxygen saturation.


* Evaluate heart sounds, cardiac rate and rhythm, and BP.


* Assess renal function: glomerular filtration rate, serum creatinine, 24-hour urine for protein, creatinine clearance, sediment, and hematuria. Eosinophilia and eosinophiluria are hallmarks of TIN.


* Assess fluid balance: fluid intake and output, daily weight, fluid retention, and electrolytes.


* Determine the presence of anemia: reduced RBCs, hemoglobin, and hematocrit from CKD resulting from low production of erythropoietin. Encourage foods rich in iron.


* Assess for shortness of breath, fever, fatigue, anorexia, nausea, and vomiting.


* Encourage the patient to spread activities evenly throughout the day to conserve energy.


* Assess if the patient can engage in activities of daily living and their quality of life.



Correlating patient-centered data and identifying priority nursing interventions will promote the best outcomes when a patient is experiencing acute illness or attempting to cope with chronic illness.




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Caravaca-Fontan F, Fernandez-Juarez G, Praga M. Acute kidney injury in interstitial nephritis. Curr Opin Criti Care. 2019;25(6):558-564.


Meyers CM, Perazella MA. Chronic tubulointerstitial nephritis. In: Gilbert SJ, Weinter DE, Bomback AS, Perazella MA, Tonelli M, eds. National Kidney Foundation's Primer on Kidney Diseases. 7th ed. New York, NY: Elsevier; 2018: 404-411.


Perazella MA. Clinical approach to diagnosing acute and chronic tubulointerstitial nephritis. Adv Chronic Kidney Dis. 2017;24(2):57-63.