Nephritis is an older term used to clinically denote a child with hypertension, decreased renal function, hematuria, and edema. Technically, nephritis suggests a noninfectious inflammatory process that involves the nephron; glomerulonephritis (GN) generally is a more precise term.
Diseases that produce GN are usually classified as primary (ie, diseases in which the kidney is the primarily affected organ) and secondary (ie, systemic disorders that involve the kidneys in addition to other organs, such as systemic lupus erythematosus [SLE]).
Currently, most children with hematuria and decreased renal function who do not have a presentation consistent with postinfectious GN receive a renal biopsy, leading to a specific pathologic diagnosis. The general terms GN and nephritis are not specific enough to be very useful for treatment or prognosis.
For a more complete discussion of poststreptococcal GN, see Acute Poststreptococcal Glomerulonephritis.
A second use of the term nephritis is to describe tubulointerstitial nephritis (TIN). TIN is a group of unrelated inflammatory disorders that initially affect mainly the interstitium and renal tubules.


In general, nephritis (ie, nonsuppurative) is produced by antigen-antibody complexes (or some other unknown mechanism) trapped in the renal parenchyma. A process of inflammation and cell proliferation (ie, endothelial, mesangial, or epithelial cells are stimulated to proliferate in varying degrees) is initiated, which damages normal renal tissue. If the inflammatory process is turned off, such as in acute poststreptococcal GN, recovery occurs. If the inflammatory process continues unabated, progressive loss of glomeruli and nephrons occurs (eg, in membranoproliferative GN).
In children with TIN, some stimulus (eg, infection, drug, metabolic abnormality) initiates a tubulointerstitial inflammatory process, leading to a mononuclear cell infiltrate. TIN is often clinically classified as acute or chronic based on the rapidity with which decreased renal clearance function develops. With acute TIN, treatment or removal of the stimulus leads to resolution. In chronic TIN, differing rates of progressive renal damage persist.

Causes of Nephritis

  • Infection of the throat.
  • Rheumatic fever or scarlet fever is usually followed by nephritis.
  • Wrong dietary habits, excessive drinking, and habitual use of chemical agents.
  • Frequent use of painkillers and suppressive medical treatment are the main causes.
  • Nutritional deficiencies also contribute.

Symptoms of Nephritis

  • Pain in the kidney that extends till the urethra.
  • Highly colored scanty urine.
  • Dull pain in the back and fever.
  • Puffiness in the face, swollen ankles and feet are the main symptoms.
  • In chronic cases patient may develop uremia, frequent urination during night and rise in Blood Pressure are other symptoms.


  • The most helpful laboratory studies include assessment of electrolyte, creatinine, and BUN levels; CBC count; urinalysis; urine culture; lupus serologies; measurement of complement components (ie, C3, C4); antistreptolysin-O (ASO) titer; anti-DNAase B, perinuclear antineutrophil cytoplasmic antibody (P-ANCA) measurement; cellular antineutrophil cytoplasmic antibody (C-ANCA) assessment; and serum IgA measurement.
    • If the child has a history consistent with acute poststreptococcal glomerulonephritis (GN), such as low C3, positive ASO, and anti-DNAase B, a provisional diagnosis of acute poststreptococcal GN can be made. Supportive care and observation for improvement within 10-14 days is reasonable.
    • If a diagnosis of acute poststreptococcal GN seems unlikely, a percutaneous renal biopsy is the single most effective mechanism to arrive at a pathologic diagnosis.
    • Laboratory findings with tubulointerstitial nephritis (TIN) include hematuria, eosinophilia, sterile pyuria, low-grade proteinuria, eosinophiluria, and urinary white blood cell casts.
    • A percutaneous renal biopsy is the criterion standard for diagnosing TIN.
  • With TIN, the hallmarks of GN (ie, edema, hypertension, sodium chloride retention) are not present. Tubular dysfunction is the predominant feature.
  • The pattern of tubular dysfunction that develops depends on the tubular segment(s) involved. Proximal tubular lesions result in aminoaciduria, glucosuria, phosphaturia, uricosuria, beta2 microglobinuria, and bicarbonaturia, often producing proximal renal tubular acidosis. Lesions involving the distal tubule result in inability to acidify the urine (distal renal tubular acidosis), to regulate sodium balance, and to secrete potassium. Lesions affecting the medulla and papilla result in inability to concentrate the urine.
  • These tubular functions may be tested by calculating the fractional excretion of phosphate or bicarbonate, measuring the urinary glucose excretion, and measuring the urine pH and osmolality with fasting.
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), anatomic abnormalities, tumor, and stones. The kidneys are frequently echodense when GN is present. The kidneys may be abnormally large or small.
  • No imaging tests are sensitive or specific for TIN. Renal ultrasonography may show large kidneys with normal echogenicity. Gallium scanning may reveal increased uptake.

  • If a specific diagnosis is needed for a child with hematuria, proteinuria, edema, and hypertension (ie, nephritis), a percutaneous renal biopsy usually is the criterion standard for identifying a specific pathology.
  • The kidney biopsy findings are diagnostic for TIN.
Histologic Findings

  • In GN, light microscopy usually reveals infiltration of the kidney by lymphocytes, polymorphonuclear leukocytes, or both. Immunofluorescence microscopy may reveal immunoglobulin G (IgG), IgA, immunoglobulin M (IgM), or complement in mesangial or vascular distribution, depending on the type of nephritis. Electron microscopy may reveal deposits in mesangial, subendothelial, subepithelial, or a combination of tissues, depending on the type of nephritis present. Replacement of renal tissue by scar tissue (tubular atrophy and interstitial fibrosis) is the final common pathway for several types of GN.
  • For TIN, light microscopy reveals focal interstitial infiltrates of edema that contains lymphocytes and eosinophils. Tubular injury is usually greater than glomerular or vascular injury.


Medical Care

Medical care for glomerulonephritis (GN) is usually divided into 2 major components: treatment of primary pathology and supportive care. In renal diseases, supportive care involves managing hypertension and fluid and electrolyte abnormalities and managing decreased renal function.
Treatment of primary pathology ranges from watchful waiting, as in postinfectious GN, to treatment with immunosuppressive medication, such as steroids or cyclophosphamide in lupus or tubulointerstitial nephritis (TIN). To discuss the primary treatment of all forms of nephritis is beyond the scope of this article. In some causes, for example IgM nephropathy, no definitive therapy is known.
Hypertension can be managed with antihypertensives, such as calcium channel–blocking agents, ACE inhibitors, angiotensin receptor–blocking agents, peripheral vasodilators, and diuretics. The most common fluid abnormality is hypervolemia managed with fluid restriction and diuretics or dialysis if renal function is too poor to respond to diuretics. Hyponatremia is usually dilutional and responds, at least partially, to removal of excess fluid. Hypocalcemia may respond to oral or intravenous calcium, depending on severity. Mild metabolic acidosis may be present but rarely requires primary treatment. For dosages of the above medications see Medication.
The primary treatment for TIN is to stop the offending agent.
Surgical Care

If dialysis access is necessary, consultation with a surgeon may be required.

Primary care physicians can usually manage children with poststreptococcal GN unless dialysis is imminent. Refer children with other forms of GN or TIN to a pediatric nephrologist.

In children with acute renal failure secondary to GN who have lost the ability to excrete a water load, fluid restriction may prevent fluid overload. TIN usually produces nonoliguric ARF. Fluid restriction of 300 mL/m2/d plus losses may allow management of acute renal failure for 2-3 days without dialysis. In patients with hypertension, sodium restriction to recommended daily allowances (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.

In patients with hypertension and renal failure, discourage strenuous activity; however, walking, playing, and other activities are acceptable.


Medications used to treat patients with glomerulonephritis (GN) generally fall into 3 categories: antihypertensives, diuretics, and anti-inflammatory or immunosuppressives.
Some recommend a short course of steroids or cyclophosphamide for tubulointerstitial nephritis. These drugs are usually not necessary. Most often, stopping the offending agent leads to recovery.
Pharmacotherapy may include numerous drug classes that have antihypertensive effects. They possess different pharmacological actions. Thiazide diuretics and beta-blockers have been the mainstay of drug therapy for hypertension. Recently, the availability of other drugs (eg, calcium-channel blockers, ACE inhibitors, alpha-blockers, angiotensin II receptor antagonists) allows regimens to be customized to the population treated and allows enhanced compliance and improved ability to tolerate treatment. For complete information, see the following pediatric topics Hypertension and Neonatal Hypertension.
Diuretic agents
These agents are used to remove excess fluid in children with edema secondary to renal disease and as an adjunct to manage hypertension.
Furosemide (Lasix)
A loop diuretic. Often effective in removing fluid even when GFR is reduced secondary to nephritis.
Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.


  • Provide best rest during the acute phase.
  • Perform passive range of motion exercises for the patient on bed rest.
  • Allow the patient to resume normal activities gradually as symptoms subside.
  • Consult the dietician about a diet high in calories and low in protein, sodium, potassium, and fluids.
  • Protect the debilitated patient against secondary infection by providing good nutrition and hygienic technique and preventing contact with infected people.
  • Check the patient’s vital signs and electrolyte values.
  • Monitor intake and output and daily weight.
  • Report peripheral edema or the formation of ascites.
  • Explain to the patient taking diuretics that he may experience orthostatic hypotension and dizziness when he changes positions quickly.
  • Provide emotional support for the patient and his family.
  • If the patient is scheduled for dialysis, explain the procedure fully.


Further 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). These problems are infrequent in the general pediatric population.
Further Outpatient Care

  • Outpatient care is an extension of inpatient care.
  • Outpatient care may be as simple as observation in a child with tubulointerstitial nephritis or resolving poststreptococcal glomerulonephritis (GN) or may involve antihypertensives, diuretics, and diet modification as in a child with IgA nephropathy or membranoproliferative GN and preserved renal function.
  • Outpatient care may involve dialysis and transplantation in a child who develops end-stage renal disease.
Inpatient & Outpatient Medications

  • No specific change in medications is necessary for transition from inpatient to outpatient care.

  • A physician who has experience in managing renal failure in children should care for children with renal failure. In the United States, this is frequently at a tertiary facility.

  • No effective methods of deterrence or prevention are known.

  • Primary complications associated with hypertension
    • Seizure
    • Encephalopathy
    • Stroke
    • End-organ damage
  • Primary complications associated with kidney failure
    • Fluid overload
    • Electrolyte abnormality
    • Uremic symptoms
    • Anemia
    • Abnormal bone mineralization
    • Sexual dysfunction
    • Poor growth
    • Anorexia
    • Endocrine abnormalities

  • The overall prognosis for survival in children with all forms of nephritis is good.
Patient Education

  • Education about the specific nephritis is helpful.
  • Encourage medication compliance and a healthy lifestyle (eg, ideal body weight, no smoking, exercise, avoidance of risk behaviors).
  • For excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center. Also, see eMedicine's patient education article Blood in the Urine.

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