Nephritis refers to inflammation of the kidney tissue. Depending on the part of the kidney affected, several distinct clinical forms are described: interstitial nephritis (involvement of the interstitial tissue between the tubules), pyelonephritis (infection-related involvement of both the renal pelvis and the renal parenchyma), and glomerulonephritis (involvement of the glomeruli).
According to the HAS, the French Society of Nephrology, and Inserm, nephritis can be acute (rapid progression, sometimes reversible) or chronic (slow progression, risk of progressive impairment of kidney function). Clinical manifestations vary depending on the form: lower back or flank pain, fever, nausea, changes in urine output, blood or protein in the urine, and high blood pressure. Nephritis is part of the family of urinary disorders whose evaluation falls strictly within the purview of medical and nephrological expertise.
The causes of nephritis are numerous and directly influence the choice of treatment. Three main mechanisms are traditionally distinguished.
Infectious causes primarily include acute pyelonephritis, a bacterial kidney infection (most commonly caused by Escherichia coli) that sometimes complicates an untreated lower urinary tract infection. Certain viral infections may also be responsible. Drug- and toxin-induced causes account for a significant proportion of interstitial nephritis cases: antibiotics (beta-lactams, sulfonamides, vancomycin, rifampin), nonsteroidal anti-inflammatory drugs (NSAIDs), proton pump inhibitors, certain antivirals, iodinated contrast agents, and prolonged self-medication. Autoimmune and systemic causes include lupus nephritis (kidney involvement in systemic lupus erythematosus), Berger’s disease (IgA nephropathy), vasculitides (particularly ANCA-associated), Gougerot-Sjögren syndrome, and certain autoimmune hepatitis. A medical reassessment of current treatments may be necessary in cases of identified drug-induced nephritis.
The diagnosis of nephritis is based on a structured approach combining clinical findings, laboratory tests, imaging, and sometimes histology. It falls strictly within the purview of a nephrologist.
The medical history takes into account potential triggers: recent medication use, infections, a history of autoimmune diseases, and exposure to toxins. The physical examination assesses blood pressure and checks for edema and systemic signs. Standard laboratory tests include: urinalysis (dipstick test for proteinuria, hematuria, and leukocyturia; urine culture if an infection is suspected), 24-hour proteinuria or protein-to-creatinine ratio in a single sample, serum creatinine and urea with estimation of glomerular filtration rate (GFR), serum electrolyte panel, complete blood count, and CRP. Depending on the clinical context, an immunological workup is performed: antinuclear antibodies, ANCA, anti-MBG, complement (C3, C4), and serum protein electrophoresis.Renal ultrasound assesses the size and morphology of the kidneys. A renal biopsy, performed in a hospital setting under ultrasound guidance, may be essential to accurately identify the histological type of nephritis and tailor treatment accordingly.
Treatment for nephritis is strictly etiological and depends on the identified cause. It requires a medical prescription, most often within a specialized nephrology setting.
For infectious nephritis (particularly pyelonephritis), targetedantibiotic therapy based on antibiotic susceptibility testing is the standard of care and should be initiated promptly after bacteriological cultures are taken. For drug-induced nephritis,the immediate discontinuation of the offending medication is the priority, sometimes combined with a short course of corticosteroids. For autoimmune nephritis (lupus nephritis, vasculitic nephritis, primary glomerulonephritis), treatment relies on systemic corticosteroids and immunosuppressants (cyclophosphamide, mycophenolate mofetil, azathioprine, rituximab, belimumab, as indicated) according to specific protocols. Management of symptoms and complications is essential: blood pressure control (often with ACE inhibitors or ARBs), reduction of proteinuria, fluid and electrolyte balance, and nutritional management. In severe cases, extrarenal blood purification may be necessary. Self-medication, particularly with NSAIDs, is strongly discouraged and may worsen the condition.
Preventing nephritis relies on limiting identified risk factors and closely monitoring high-risk situations. While it does not eliminate all cases, it significantly reduces their incidence.
Several preventive measures are recommended. Limit the use of NSAIDs and prolonged self-medication, particularly in vulnerable individuals (the elderly, those with hypertension, those with diabetes, and those who are dehydrated). Maintain adequate hydration and avoid prolonged dehydration. Promptly treat lower urinary tract infections to prevent their progression to complicated cystitis and pyelonephritis. Effectively manage underlying chronic conditions —such as diabetes, hypertension, and systemic autoimmune diseases (lupus, vasculitis)—under regular medical supervision. Conduct regular nephrological follow-up for at-risk individuals: older adults on multiple medications, patients with diabetes, patients with a personal or family history of kidney disease, and patients on long-term nephrotoxic treatments. For urinary comfort support, the pharmacy offers appropriate products, though these are not a substitute for medical care.
Untreated or inadequately managed nephritis can lead to several complications, some of which may be serious. Prompt medical consultation and regular monitoring can help prevent these complications.
Progression to chronickidney disease is the most feared outcome, involving a gradual and often irreversible loss of kidney function. Acute kidney injury may occur in severe cases and require emergency dialysis.High blood pressure, which is frequently associated with kidney disease, complicates the situation and requires specific treatment. Electrolyte imbalances (hyperkalemia, metabolic acidosis) can complicate severe cases. Progression to severe uremia and nephrotic syndrome (massive proteinuria, hypoalbuminemia, edema) is possible in certain forms of the disease. In the long term, end-stage chronic kidney disease may require dialysis or a kidney transplant. Any new symptoms (fever, widespread edema, severe lower back pain, changes in urine output) should prompt a prompt medical consultation.
Regular nephrologic follow-up is essential for patients diagnosed with nephritis. It is key to adjusting treatment and preventing long-term complications.
This monitoring serves several key purposes.Assessing treatment effectiveness through regular monitoring of kidney function (serum creatinine, estimated glomerular filtration rate [eGFR]), proteinuria, and inflammatory markers.Adjusting treatment based on the patient’s progress and the side effects of immunosuppressive or other therapies. Monitoring blood pressure, a key factor in kidney protection. Early detection of complications or relapses, which are characteristic of certain autoimmune forms.Adjustment of other treatments to avoid nephrotoxic medications (NSAIDs, certain antibiotics, and iodinated contrast agents, which should be avoided whenever possible). Follow-up is generally coordinated among the primary care physician, the nephrologist, and any other specialists (a rheumatologist for lupus, a urologist as needed). The frequency of follow-up visits depends on the severity of the disease and the phase of care (initial, stabilization, maintenance).
Although both terms refer to kidney inflammation, nephritis (in the strict sense of interstitial nephritis) and glomerulonephritis affect different structures of the kidney. This distinction is essential for diagnosis and treatment.
Interstitial nephritis affects the interstitial tissue of the kidney—that is, the supportive tissue located between the tubules. The main causes are drug-related (NSAIDs, antibiotics, PPIs), toxic, infectious, or autoimmune. Proteinuria is often moderate, and tubular function may be impaired. Glomerulonephritis affects the glomeruli, small filtration units located in the renal cortex that filter the blood. The causes are primarily autoimmune (lupus, IgA nephropathy, Goodpasture syndrome) or post-infectious. It often manifests as marked proteinuria (sometimes nephrotic syndrome), hematuria, and impaired glomerular filtration rate. Pyelonephritis, the third condition, is a bacterial infection of the renal parenchyma and renal pelvis, distinct from the previous two. An accurate differential diagnosis relies on laboratory tests, imaging, and often a renal biopsy, which remains the gold standard for identifying the exact form of the disease.
Recovery from nephritis depends largely on its cause, the speed of diagnosis, and the quality of treatment. The prognosis varies considerably depending on the specific form.
Acute nephritis of infectious origin (uncomplicated pyelonephritis) that is properly treated with appropriate antibiotic therapy can resolve without sequelae in the majority of cases. Drug-induced nephritis detected early and followed by discontinuation of the offending medication is often reversible, sometimes without sequelae, although impaired kidney function may persist. Autoimmune nephritis (lupus nephritis, primary glomerulonephritis, vasculitis) are chronic diseases that generally require long-term management with immunosuppressants. Complete remission is possible, but relapses may occur and require prolonged monitoring. Unfortunately, chronic progressive forms may progress to end-stage chronic kidney disease despite treatment. The individual prognosis varies widely and can only be determined by the treating nephrologist based on the precise diagnosis, initial severity, response to treatment, and comorbidities.
Diet plays an important role in the management of nephritis, particularly when kidney function is impaired. Dietary adjustments should be tailored in consultation with the nephrologist and, ideally, a dietitian specializing in nephrology.
Several principles guide dietary adjustments. Limit salt intake (generally less than 6 g/day) to reduce sodium load and control blood pressure. Adjust protein intake according to the stage of the disease: moderate restriction in chronic kidney disease (without deficiency), and maintenance of intake in cases of nephrotic syndrome. Monitor potassium intake in cases of impaired kidney function, and restrict it in cases of hyperkalemia (dried fruit, bananas, chocolate, and certain vegetables should be limited as prescribed). Adjust phosphorus intake in advanced stages (dairy products, deli meats, phosphate-rich sodas). Hydration should be tailored to urine output—neither too restrictive nor excessive—depending on the clinical context.Avoiding over-the-counterNSAIDs is an essential measure. To support urinary tract health and waste elimination, the pharmacy offers appropriate products in accordance with medical guidance.
Nephritis, particularly in its chronic or autoimmune forms, can significantly affect quality of life. Taking this impact into account is an integral part of patient care.
Several aspects of life may be affected. Chronic fatigue, which is particularly severe in autoimmune diseases and chronic kidney disease, impacts daily and professional activities. Therapeutic constraints (taking multiple medications, side effects of corticosteroids and immunosuppressants, and regular medical follow-up) can weigh heavily on daily life. Dietary restrictions—particularly regarding sodium, potassium, and phosphorus—require adaptation and learning. Psychological effects (anxiety and, at times, symptoms of depression in the face of a chronic illness) are common and warrant support from a psychologist or psychiatrist if needed. Work-related limitations may require workplace accommodations. Social and community support (patient organizations such as Renaloo and France Rein) provides valuable assistance. Multidisciplinary care (nephrologist, primary care physician, dietitian, psychologist, social worker) optimizes overall quality of life.
Research in nephrology is actively progressing, with several recent therapeutic advances that are gradually transforming the management of nephritis, particularly autoimmune nephritis.
Several areas of progress stand out. Targeted biologic therapies (monoclonal antibodies such as rituximab, belimumab, and obinutuzumab for lupus nephritis) offer greater specificity of action and a side effect profile that is often more favorable than that of conventional immunosuppressants. Complement pathway inhibitors (eculizumab, ravulizumab) have revolutionized the treatment of certain rare forms of glomerulonephritis (notably atypical hemolytic-uremic syndrome). SGLT2 inhibitors (dapagliflozin, empagliflozin), initially developed for diabetes, have demonstrated significant renal benefit in several chronic kidney diseases with proteinuria. Nonsteroidal mineralocorticoid receptor antagonists (finerenone) are indicated for certain patients with chronic kidney disease and diabetes. Research continues in the areas of cell therapies and personalized medicine. These innovations remain strictly prescribed within the framework of validated nephrology protocols and under close medical supervision.
