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Introduction   

Interstitial nephritis (IN) is a common occurrence that can present itself in the emergency room, ICU, Med-Surg floor, or even in the outpatient setting. Nurses in all of these settings need to understand how these patients present, and which therapies and management strategies are utilized.  

IN is seen in 1-7% of all diagnostic kidney biopsies performed worldwide and in 27% of kidney biopsies performed when acute kidney injury (AKI) is suspected (2). The incidence of acute IN is rising yearly, especially in the elderly population, which in turn points to the significance of nurses being educated and informed about this condition.  

Definition 

Interstitial nephritis (IN) is a kidney disease that decreases the patient’s ability to clean the blood and produce urine. More specifically, an inflammatory infiltrate is present in the interstitium of the kidneys, and a decline in kidney function presents itself. The tubules of the kidneys and the interstitium all become inflamed as a result (2)(3)(6).  

The term interstitial nephritis (IN) has been known for several years in the medical community, and while this term is commonly used, tubulointerstitial nephritis more accurately describes this disease since the interstitium and the tubules are involved in the disease process (4). These terms will be used interchangeably in this article.  

Etiology 

Understanding the causes of IN is important to determine the course of treatment and management for patients. IN has multiple etiologies including diseases, toxins, and medications that damage the kidney’s interstitium (6). The most common form of tubulointerstitial inflammation in IN is a hypersensitive reaction to medications which is known as allergic IN.  

IN can either be acute or chronic, and listed below are both acute and chronic causes (1):  

Acute 

• Hypersensitivity reactions: Any medication can cause an allergic reaction involving the kidneys. 
  • The most common medications that can cause a reaction are antibiotics (quinolones, sulfa drugs, cephalosporins, and penicillin), NSAIDs, proton pump inhibitors, rifampin, phenytoin, interferon alfa, allopurinol, and diuretics (furosemide, thiazides) 
• Acute transplant rejection 
• Immunologic diseases such as Goodpasture syndrome and lupus 
• Infections (including bacterial, viral, fungal or parasitic) 

Chronic 

• Drugs (i.e., lithium, analgesics, tacrolimus, cyclosporine) 
• Heavy metals (mercury, lead, cadmium) 
• Obstructive uropathy, reflux disease, nephrolithiasis  
• Immunologic diseases (i.e., vasculitis chronic transplant nephropathy, lupus) 
• Neoplasia (i.e., leukemia, myeloma) 
• Ischemic atherosclerotic kidney disease (i.e., dyslipidemia, smoking, catheter manipulations above the level of the renal arteries) 
• Metabolic diseases (i.e., potassium depletion, hypercalcemia, hyperoxaluria) 
• Genetics (i.e., medullary cystic disease and amyloidosis, and Alport syndrome) 
• Miscellaneous (i.e., Chinese herb/aristolochic acid nephropathy, Balkan endemic nephropathy)  

(1) 

Epidemiology 

Primary tubulointerstitial diseases (i.e., diseases of the interstitium without glomeruli involvement and renal tubules) make up 10-15% of all kidney diseases in the United States and around the world. Acute or chronic tubulointerstitial diseases are not higher in any particular race. It can be noted, however, that analgesic nephropathy is 5-6 times more common in women than in men because women typically ingest more analgesics than men do. (1)  

As mentioned previously, drug-induced acute interstitial nephritis (AIN) is the main etiology of reported cases, followed by infections and immunological diseases. Among drug-induced AIN, antibiotics are the most frequent causative medication followed by NSAIDs and proton-pump inhibitors (PPIs) (2). Understanding the epidemiology of IN is important for nurses to obtain a thorough patient health history, perform an in-depth physical examination, and recognize the steps of treatment and management.  

Pathophysiology 

IN is comprised of immune-mediated infiltration of the interstitium of the kidneys by inflammatory cells. This injury leads to the expression of new local antigens, activation of proinflammatory and chemoattractant cytokines, and inflammatory cell infiltration. The cytokines are produced by the macrophages and lymphocytes (inflammatory cells) as well as the fibroblasts, vascular endothelial and interstitial cells, and proximal tubules (kidney cells). (1) 

All these inflammatory changes lead to either acute or chronic IN. 

Presenting Signs and Symptoms 

Understanding the presenting signs and symptoms of acute and chronic IN is important for nurses to harness the ability to recognize this potential diagnosis and aid in the patient’s clinical improvement. IN can cause mild to severe kidney problems including but not limited to acute kidney injury (AKI) (7). In about 50% of cases, patients will have oliguria (decreased urine output) in addition to other signs of AKI.  

Additional symptoms may include:  

• Hematuria  
• Fever 
• Increased urine output 
• Mental status changes (coma, confusion, drowsiness) 
• Nausea 
• Vomiting 
• Rash 
• Swelling in any area of the body 
• Weight gain from fluid retention  
• Hypertension  
• Flank pain  
• Pyuria 
• Maculopapular rash 
• Arthralgia 

(1)(5)(7) 

Clinical Work-up and Diagnosis  

To correctly diagnose patients, providers will perform an array of laboratory and diagnostic exams on potential IN patients to develop a diagnosis. Laboratory evaluations include a CBC with differential, urine studies (urinalysis), chemistry panel, liver function tests, and IgE levels (1)(4).  

Diagnostic evaluations may include Ultrasound, KUB x-ray, CT scan, EDTA lead mobilization tests as well as a kidney biopsy and histologic features.  

The following laboratory findings may assist providers in making the diagnosis of IN:  

• Eosinophilia 
• Anemia 
• Proteinuria 
• Pyuria 
• Hematuria 
• Renal casts or tubular epithelial cells  
• Eosinophiluria  
• Low bicarbonate level 
• Hyperkalemia 
• Elevated BUN  
• Elevated Creatinine  
• Elevated serum transaminase levels 
• Elevated IgE (serum) levels  

(1)(4) 

Of the diagnostic tests used to diagnose IN, it should be noted that the gold standard for diagnosing acute IN is a kidney biopsy. This test is usually done when the diagnosis is still unclear and there are no contraindications of the procedure (4)(5).  

The following imaging study findings may assist providers in the diagnosis of IN:  

• Enlarged kidney size 
• Hydronephrosis 
• Increased cortical echogenicity 
• Positive gallium 67 scans 
• Plasma cell and lymphocytic infiltrates, mononuclear, eosinophilic cellular infiltration, fibrosis, and atrophy present on renal biopsy  
• Renal papillary tips present on CT scan  

(1)(4) 

Treatment 

The most important step in the treatment of AIN is withholding the particular offending agent if possible (1)(5). Early recognition and cessation of the offending medication will typically result in a complete recovery for the patient (1). If there is no sign of improvement in patients within a few days of discontinuation, steroid therapy is considered. The typical dose is prednisone 1 mg/kg for 4-6 weeks with a rapid taper regimen (1)(5). Additionally, in the case of infectious IN, the infection is treated with the use of non-nephrotoxic antibiotic regimens.  

For chronic cases of IN, the treatment depends on the causative factors and will consist generally of supportive measures, blood pressure control, and anemia management (1).  

Prognosis 

Fortunately for most patients, the prognosis of IN is fairly good. The majority of patients in which the offending drug or medication is removed early are typically expected to recover to normal or near-normal kidney function within a few weeks (4). In rare cases, IN can cause permanent damage which could include chronic kidney failure. AIN can be more severe and has an increased likelihood of progressing to long-term or permanent kidney damage in the elderly (7).  

Supportive care and Nursing interventions  

Nursing care and supportive care measures for IN focus on alleviating symptoms, preventing complications, and promoting kidney function recovery. Supportive care measures for the healing patient include but are not limited to:  

• Maintaining adequate hydration 
• Fluid and electrolyte management 
• Symptomatic relief for rashes 
• Avoiding volume depletion or overload 
• Symptomatic relief for fever and/or systemic symptoms 
• Avoiding the use of nephrotoxic drugs  
• Avoiding the use of drugs that impair renal blood flow  
• Adjusting drug dosages for existing levels of renal function  

(1)(4) 

Nurses will play a crucial role in monitoring patients’ vital signs, fluid balance, and electrolyte levels. Administering prescribed medications, such as corticosteroids, antipyretics, or antibiotics, and ensuring adherence to the treatment regimen are essential duties.  

Educating patients about dietary restrictions, especially reducing sodium and protein intake, can help manage IN. Regular monitoring for signs of infection or worsening renal function is necessary to promptly address any complications. Emotional support and patient education about the condition and its management encourage patients to actively participate in their care and improve outcomes. 

Conclusion

In conclusion, nursing care for patients with IN is critical in managing the condition and improving patient outcomes. By understanding the underlying mechanisms, recognizing the clinical signs, and implementing appropriate supportive care measures, nurses can significantly impact patient recovery and healing.  

Comprehensive care for IN involves continuous patient monitoring, effective symptom management, patient education, and patient advocacy. By supporting patients with IN in these ways, nurses can help in improving patient outcomes overall.  

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