Glomerulonephritis and Nephrotic Syndrome

Glomerular diseases damage the kidney's microscopic filters and can cause blood, protein or both to leak into urine. A nephritic presentation centres on haematuria, hypertension and variable kidney impairment, while nephrotic syndrome combines heavy proteinuria, low blood albumin, oedema and hyperlipidaemia. These patterns overlap, and rapidly progressive kidney failure or lung bleeding requires emergency specialist care.

What the glomerulus does Each kidney contains about a million microscopic filtering units called nephrons. Every nephron begins with a glomerulus, a small tuft of capillaries enclosed by Bowman's capsule. Blood enters the glomerulus under pressure. Water and selected small molecules cross the filtration barrier into Bowman's space, while blood cells and most large proteins remain within the circulation. The filtered fluid then enters the kidney tubule. The tubule returns needed water, salts, glucose and other substances to the blood and removes additional waste before urine leaves the kidney. Glomerular disease therefore affects the first filtration step. Tubular or interstitial disease mainly affects the processing of fluid after filtration, although severe kidney disorders often involve more than one compartment. The glomerular filtration barrier The filtration barrier has three closely connected layers. These are the fenestrated capillary endothelium, the glomerular basement membrane and the slit diaphragm between podocyte foot processes. The barrier selects substances partly by size, shape and electrical properties. Albumin is a relatively large negatively charged protein and is normally retained efficiently. Damage to the barrier can allow albumin, other proteins and red blood cells to enter urine. The amount and type of leakage depend on which part of the barrier is affected. A normal looking kidney on ultrasound can still have serious glomerular disease because the abnormality may be microscopic. Podocytes and the slit diaphragm Podocytes are specialised cells covering the outside of glomerular capillaries. Their interlocking foot processes create narrow filtration slits. Proteins including nephrin and podocin help maintain the slit diaphragm. Injury to podocytes is central to minimal change disease, focal segmental glomerulosclerosis and several inherited nephrotic disorders. Podocytes have limited ability to replace themselves. Persistent loss or detachment can lead to scarring within glomeruli. This explains why reducing protein leakage is not only about improving urine appearance. It can help protect remaining glomerular structure over time. How glomerular disease differs from tubular and interstitial disease Glomerular disease commonly produces albumin rich proteinuria, haematuria with dysmorphic red cells and red cell casts. Tubular disease more often impairs urine concentration, acid handling and electrolyte transport. It can produce low molecular weight proteinuria, glucose in urine despite normal blood glucose or abnormal potassium and bicarbonate. Interstitial disease can cause white cells in urine, impaired concentration and acute kidney injury. Medicines and infection are common triggers of acute interstitial nephritis. These distinctions guide investigation, but they are not absolute. A severe glomerular disorder can injure tubules secondarily, and a systemic disease can affect several kidney compartments. What glomerulonephritis means Glomerulonephritis means inflammation or immune mediated injury affecting glomeruli. It is a group of disorders rather than one diagnosis. Causes include IgA nephropathy, lupus nephritis, infection related disease, ANCA associated vasculitis and anti GBM disease. Some conditions traditionally grouped with glomerulonephritis cause little visible inflammation. Membranous nephropathy and minimal change disease are examples of glomerular diseases that often present through protein leakage. The exact diagnosis matters because treatment ranges from supportive care alone to urgent plasma exchange and immunosuppression. Clinical syndromes are patterns, not biopsy diagnoses Doctors often describe a nephritic pattern or nephrotic syndrome before the underlying disease is known. These terms summarise findings from symptoms, blood pressure, urine and blood tests. They help prioritise risks and investigations. They do not identify one specific microscopic cause. Several diseases can produce either pattern, and the same disease can present differently in different people. Kidney biopsy often converts the clinical pattern into a pathological diagnosis that can guide treatment and prognosis. The nephritic presentation A nephritic presentation is dominated by glomerular inflammation and blood leakage. Typical features include microscopic or visible haematuria, dysmorphic red blood cells, red cell casts, hypertension and variable loss of kidney function. Proteinuria is common but may be below nephrotic range. Salt and water retention can cause oedema and breathlessness. Urine may look smoky, tea coloured or cola coloured. The presentation can be mild and chronic or rapidly progressive over days to weeks. Red blood cells and red cell casts Red cells squeezed through a damaged glomerular barrier can become misshapen. These are called dysmorphic red cells or acanthocytes. Within kidney tubules, red cells can become embedded in a protein matrix and form red cell casts. A cast has the shape of the tubule in which it formed. Red cell casts strongly support bleeding from within the kidney, particularly glomerular inflammation. They are not expected from an uncomplicated bladder infection or ordinary menstrual contamination. Their absence does not exclude glomerulonephritis because casts can be intermittent and microscopy quality varies. What nephrotic syndrome is Nephrotic syndrome is the clinical consequence of severe glomerular protein leakage. The classic constellation is heavy proteinuria, low serum albumin, oedema and hyperlipidaemia. Frothy urine and weight gain from fluid are common. In adults, nephrotic range proteinuria is often defined as more than 3 to 3.5 grams daily or a urine protein to creatinine ratio around or above 300 to 350 milligrams per millimole. Thresholds vary with age and laboratory practice. The syndrome is defined by the complete pattern rather than one isolated dipstick result. Heavy proteinuria Proteinuria means an abnormal amount of protein in urine. Albumin is the main protein lost in many glomerular diseases. Urine dipsticks are useful screening tools but become less reliable at very high concentrations and mainly detect albumin. A spot urine protein to creatinine ratio estimates total daily protein loss without requiring a full 24 hour collection. An albumin to creatinine ratio measures albumin specifically and is widely used in chronic kidney disease assessment. Protein excretion varies through the day and during fever, exercise and acute illness. Important results are confirmed and followed sequentially. Hypoalbuminaemia Albumin helps maintain oncotic pressure, transports several substances and contributes to antioxidant and other functions. When urinary loss exceeds liver replacement, the serum albumin falls. Inflammation, liver disease, poor intake and dilution can also lower albumin. A low albumin in someone with heavy proteinuria supports nephrotic syndrome, but the albumin concentration does not measure kidney function directly. Very low albumin is associated with greater oedema and thrombotic risk, although the complete clinical context determines management. Why oedema develops Loss of albumin can reduce the force retaining fluid within blood vessels, allowing fluid to move into tissues. The kidneys may also retain sodium directly because glomerular and tubular signalling is altered. Both underfilling and primary sodium retention can contribute. Swelling often begins around the eyes or ankles and can progress to the legs, genital area, abdominal cavity and lungs. A person can look fluid overloaded while the effective circulating volume is low. This makes aggressive diuretic or intravenous fluid treatment potentially hazardous without careful assessment. Hyperlipidaemia The liver increases lipoprotein production in response to low oncotic pressure and altered protein metabolism. Total cholesterol, low density lipoprotein cholesterol and triglycerides can rise substantially during active nephrotic syndrome. Lipid levels may improve when proteinuria remits. Persistent elevation still contributes to long term cardiovascular risk. Lipid treatment depends on age, kidney function, expected duration of nephrosis and overall cardiovascular risk rather than the cholesterol number alone. Nephrotic and nephritic patterns are not a strict binary Nephrotic and nephritic are complementary descriptions rather than mutually exclusive diagnoses. Lupus nephritis, membranoproliferative patterns and severe IgA nephropathy can produce haematuria, impaired filtration and nephrotic range proteinuria together. Minimal change disease usually has a predominantly nephrotic presentation, while ANCA associated glomerulonephritis is usually strongly nephritic. Recognising overlap prevents a falsely reassuring assumption that heavy proteinuria means inflammation cannot be rapidly destructive. Minimal change disease Minimal change disease is the commonest cause of nephrotic syndrome in childhood, especially between early childhood and school age. The glomeruli look almost normal by light microscopy. Electron microscopy shows widespread flattening or effacement of podocyte foot processes. Most children with a typical presentation respond to glucocorticoids, so kidney biopsy is not routinely required before first treatment. Adults can also develop minimal change disease. Adult presentation more often includes acute kidney injury and usually requires biopsy confirmation. Focal segmental glomerulosclerosis Focal segmental glomerulosclerosis, shortened to FSGS, is a pattern of scarring seen on kidney biopsy. Focal means that only some glomeruli are affected. Segmental means that only part of an affected glomerulus is scarred. Primary FSGS can produce abrupt nephrotic syndrome and is thought to involve a circulating podocyte injury process in some people. Secondary FSGS develops when glomeruli adapt to reduced nephron number, obesity, reflux, sickle cell disease, viral infection, medicines or other stress. Genetic and secondary FSGS Changes in genes coding for podocyte or basement membrane proteins can cause inherited FSGS. Genetic disease is more likely with early onset, family history, steroid resistance, syndromic features or recurrence patterns that do not fit primary disease. Secondary and genetic FSGS usually do not benefit from high dose glucocorticoids used for primary FSGS. Removing the stressor and reducing intraglomerular pressure are central. Accurate classification prevents prolonged immunosuppression that is unlikely to help. Membranous nephropathy Membranous nephropathy is an important cause of nephrotic syndrome in adults. Immune deposits form beneath podocytes along the outer aspect of the glomerular basement membrane. The membrane appears thickened on microscopy. Many primary cases are associated with antibodies against the phospholipase A2 receptor, called PLA2R. Other target antigens are increasingly recognised. The course ranges from spontaneous remission to persistent nephrotic syndrome, thrombosis and progressive kidney failure. IgA nephropathy IgA nephropathy is the commonest primary glomerulonephritis worldwide. IgA containing immune complexes deposit mainly within the glomerular mesangium and trigger injury. A classic presentation is visible haematuria during or shortly after an upper respiratory infection. Many people instead have persistent microscopic blood and protein discovered on routine testing. The course is highly variable. Some people remain stable for decades, while others gradually develop chronic kidney disease. IgA nephropathy is confirmed by biopsy No blood test alone confirms IgA nephropathy. Serum IgA can be normal or raised and is not diagnostic. Kidney biopsy shows dominant or co dominant IgA deposition. Risk assessment considers proteinuria, blood pressure, estimated filtration, biopsy findings and the trend over time. Current guidance places intensive supportive care, including blood pressure and proteinuria reduction, at the centre of treatment. Additional disease specific treatment is selected according to progression risk. Post infectious glomerulonephritis Post infectious glomerulonephritis develops after or during an infection. The classic childhood pattern follows a streptococcal throat or skin infection after a delay. Modern adult cases are often associated with active staphylococcal or other infections. Features include haematuria, oedema, hypertension, reduced kidney function and low complement, particularly C3. Treatment focuses on eradicating active infection and supporting kidney and blood pressure function. Routine immunosuppression can worsen infection and is not standard. Lupus nephritis Systemic lupus erythematosus can produce several patterns of immune complex glomerular disease. Lupus nephritis may cause microscopic blood, proteinuria, nephrotic syndrome, hypertension or rapidly declining kidney function. Complement levels often fall and anti double stranded DNA antibody activity may rise, but neither replaces urine monitoring or biopsy. Kidney biopsy classifies the pattern and activity and guides the intensity of immunosuppressive treatment. ANCA associated vasculitis ANCA associated vasculitis is a group of small vessel inflammatory disorders that can cause rapidly progressive pauci immune glomerulonephritis. Examples include granulomatosis with polyangiitis and microscopic polyangiitis. Eosinophilic granulomatosis with polyangiitis can also involve kidneys. Possible clues include sinus disease, nosebleeds, hearing change, lung symptoms, purpura, nerve damage and systemic illness. ANCA blood tests support diagnosis, but ANCA can be negative or positive in other settings. Kidney biopsy often provides essential confirmation and prognostic information. Anti GBM disease Anti glomerular basement membrane disease is a rare but critical autoimmune disorder. Antibodies attack the basement membrane within glomerular capillaries. They can also attack the alveolar basement membrane in the lungs. Kidney injury can progress from mild creatinine elevation to dialysis dependence within days. Pulmonary haemorrhage can cause breathlessness, falling haemoglobin and coughing blood. Treatment is an emergency and usually combines plasma exchange, glucocorticoids and cyclophosphamide. Goodpasture's disease and pulmonary renal syndrome The term Goodpasture's disease has traditionally described anti GBM disease with both kidney inflammation and lung haemorrhage. Pulmonary renal syndrome more broadly means glomerulonephritis combined with alveolar haemorrhage. ANCA associated vasculitis is another major cause. Coughing blood may be absent despite lung bleeding. New breathlessness, low oxygen, chest infiltrates and a falling haemoglobin can provide the clue. Suspected pulmonary renal syndrome requires same day specialist and emergency assessment. Treatment should not be delayed solely while waiting for biopsy when the person is deteriorating. Diabetic kidney disease and nephrotic proteinuria Diabetes is a common cause of albuminuria and chronic kidney disease and can eventually produce nephrotic range protein loss. The usual course is gradual, particularly with longstanding diabetes, retinopathy and progressive albuminuria. Sudden nephrotic syndrome, active urine sediment, rapid kidney decline or systemic features may indicate a separate glomerular disease. A person with diabetes can therefore still need kidney biopsy when the presentation is atypical. Amyloidosis Amyloidosis occurs when abnormal protein fibrils deposit within tissues. Kidney involvement commonly causes heavy proteinuria and nephrotic syndrome. Heart, nerves, liver and other organs may also be affected. AL amyloidosis is related to an abnormal plasma cell protein. AA amyloidosis can follow prolonged inflammatory disease. Diagnosis can involve blood and urine monoclonal protein testing, tissue biopsy and specialist typing of the amyloid protein. Visible and non visible haematuria Visible glomerular haematuria can make urine look pink, red, smoky, tea coloured or cola coloured. Microscopic haematuria is detected only by dipstick and microscopy. Blood from stones, infection, bladder disease, cancer, menstruation and exercise can produce a positive dipstick. Proteinuria and dysmorphic red cells make a glomerular source more likely. Painless visible haematuria still needs appropriate urinary tract assessment even when a glomerular disorder is known. Oedema patterns Nephrotic oedema can begin around the eyelids, particularly in the morning, and later affect the ankles and legs. Severe swelling can involve the scrotum or vulva, the abdominal cavity and the pleural spaces around the lungs. Weight can rise rapidly because of fluid even while muscle and nutritional reserves fall. Breathlessness, skin breakdown, abdominal pain or reduced urine makes oedema more urgent. Hypertension Glomerular inflammation and reduced filtration can cause sodium retention and high blood pressure. Severe hypertension can produce headache, visual change, chest pain, confusion, seizures or acute pulmonary oedema. Blood pressure control helps reduce further glomerular injury and cardiovascular risk. Rapidly rising pressure with neurological or cardiac symptoms is an emergency rather than a routine outpatient adjustment. Reduced urine and acute kidney injury Glomerulonephritis can reduce filtration rapidly and cause oliguria or anuria. Creatinine may rise before severe symptoms appear. Potassium, acid and fluid can accumulate. Nephrotic syndrome can also cause acute kidney injury through low effective circulating volume, sepsis, thrombosis, medicines or severe underlying glomerular disease. The acute kidney injury pathway and glomerular investigation therefore often proceed together. Systemic clues A rash, joint pain, mouth ulcer, photosensitivity or hair loss can suggest lupus or vasculitis. Sinus inflammation, nosebleeds, hearing change, lung symptoms, foot drop or skin purpura can suggest ANCA associated vasculitis. Fever, weight loss and a heart murmur can suggest endocarditis or another infection. Cancer symptoms, neuropathy, enlarged tongue, heart failure or abnormal blood proteins can point towards amyloidosis or a monoclonal disorder. The initial history The clinician asks when swelling, urine change and blood pressure symptoms began and whether they are progressing. Questions cover infection, rash, joint symptoms, respiratory symptoms, medicines, pregnancy, diabetes, cancer and autoimmune disease. A detailed drug history includes NSAIDs, antibiotics, lithium, heroin exposure, immune therapies and over the counter products. Family history, childhood urine abnormalities, hearing loss and ancestry can identify inherited or APOL1 associated risk pathways. The physical examination The examination measures blood pressure, pulse, oxygen level, temperature and weight. The clinician assesses eyelid, leg and genital oedema, fluid in the abdomen and signs of pulmonary oedema. Skin, joints, mouth, nerves, heart and lungs are examined for systemic disease. Volume assessment is important because severe oedema does not guarantee that the circulation can tolerate aggressive diuresis. Urine dipstick Urine dipstick rapidly detects blood and estimates albumin rich protein. Leucocytes and nitrites can suggest infection. Glucose may indicate diabetes or tubular dysfunction. Dipstick blood detects haemoglobin activity and can be positive with red cells, free haemoglobin or myoglobin. A positive test is followed by microscopy and quantitative protein measurement when glomerular disease is possible. Urine microscopy Fresh urine microscopy can identify dysmorphic red cells, red cell casts, white cell casts and granular casts. Acanthocytes and red cell casts strongly support a glomerular bleeding source. White cells can accompany interstitial nephritis or infection. Granular casts can indicate tubular injury. Microscopy quality and timing matter, so a negative result does not completely exclude active glomerulonephritis. Quantifying protein with PCR and ACR A spot urine protein to creatinine ratio, or PCR, estimates total protein excretion and is useful when nephrotic syndrome is suspected. An albumin to creatinine ratio, or ACR, is more sensitive for lower levels of albumin and is central to chronic kidney disease risk assessment. Nephrotic range proteinuria in adults is commonly a PCR around or above 300 to 350 milligrams per millimole. The same unit should be used when comparing results because milligrams per gram and milligrams per millimole are not interchangeable. Blood tests Creatinine and estimated filtration assess kidney function, while serial results show the rate of change. Electrolytes and bicarbonate identify hyperkalaemia and acidosis. Serum albumin helps confirm nephrotic syndrome. Full blood count, inflammatory markers, liver tests, glucose, HbA1c and lipid profile provide context and identify complications. Calcium, phosphate, immunoglobulins and other tests are selected according to severity and suspected cause. Complement testing Complement proteins help immune defence and can be consumed during immune complex disease. Low C3 can occur in post infectious glomerulonephritis and C3 glomerulopathy. Low C3 and C4 can occur in active lupus or cryoglobulinaemia. Normal complement is common in IgA nephropathy, ANCA associated vasculitis and anti GBM disease. Complement patterns narrow the differential but do not provide a final diagnosis by themselves. Autoimmune and immunology tests ANA and anti double stranded DNA antibodies support lupus assessment. ANCA testing includes antibodies associated mainly with proteinase 3 or myeloperoxidase. Anti GBM antibody testing is urgent when rapidly progressive disease or pulmonary haemorrhage is possible. PLA2R antibodies support primary membranous nephropathy in an appropriate presentation. These tests can be falsely positive or negative. Results must be interpreted with the clinical pattern and often a kidney biopsy. Infection and monoclonal protein testing Hepatitis B, hepatitis C and HIV testing is considered according to the glomerular pattern and before immunosuppression. Blood cultures are important when endocarditis or systemic infection is possible. Serum electrophoresis, immunofixation and free light chains assess monoclonal immunoglobulin disorders, particularly in older adults or with unexplained proteinuria. Cryoglobulin testing requires careful warm sample handling to avoid a false negative result. Kidney ultrasound Ultrasound checks kidney size, anatomy and urinary obstruction. It does not diagnose the microscopic glomerular lesion. Normal sized kidneys can have severe active glomerulonephritis. Small echogenic kidneys suggest chronic scarring and can affect biopsy risk and expected treatment benefit. Ultrasound also guides the biopsy needle and helps reduce damage to nearby structures. Why kidney biopsy is often necessary Kidney biopsy remains the gold standard for diagnosing many glomerular diseases. It distinguishes minimal change disease, FSGS, membranous nephropathy, immune complex disease, ANCA associated injury and anti GBM disease. The sample can show whether lesions are active and potentially reversible or predominantly chronic and scarred. Treatment decisions involving high risk immunosuppression often depend on this distinction. When biopsy may be delayed or avoided A typical young child with first steroid sensitive nephrotic syndrome is often treated without an initial biopsy. A strongly positive PLA2R antibody with a compatible adult membranous presentation can sometimes establish the diagnosis without immediate biopsy, depending on kidney function and the clinical context. In suspected anti GBM or rapidly progressive ANCA disease, urgent treatment may begin before the biopsy result when delay threatens life or kidney recovery. Severe bleeding risk, uncontrolled hypertension or very small scarred kidneys can make biopsy unsafe or unlikely to change management. Rapidly progressive glomerulonephritis Rapidly progressive glomerulonephritis describes a rapid loss of kidney function over days to weeks with active glomerular urine findings. Biopsy often shows crescents, which form when severe capillary wall injury allows inflammatory material into Bowman's space. Major causes include ANCA associated vasculitis, anti GBM disease and severe immune complex glomerulonephritis. This is a nephrology emergency. Waiting for routine outpatient review can convert treatable inflammation into irreversible scarring. Oedema complications Severe oedema stretches skin, reduces mobility and increases the risk of pressure damage and cellulitis. Fluid in the abdomen can cause discomfort, poor appetite and breathing restriction. Pleural fluid can worsen breathlessness. Rapid diuresis can reduce effective circulating volume and precipitate acute kidney injury or thrombosis. Daily weight, urine output, blood pressure and electrolytes help guide safe removal of fluid. Why infection risk rises in nephrotic syndrome Immunoglobulins and complement related proteins can be lost in urine. Tissue oedema can impair local defence, while poor nutrition and immunosuppressive treatment add further risk. Children are particularly vulnerable to pneumococcal infection and spontaneous bacterial peritonitis. Adults can develop cellulitis, pneumonia, urinary infection and sepsis. A serious infection can occur with less obvious fever during immunosuppression. Deterioration should prompt urgent assessment. Why blood clot risk rises Nephrotic syndrome creates a hypercoagulable state through several mechanisms. Antithrombin can be lost in urine, reducing a natural anticoagulant pathway. Protein C and protein S activity can also become altered. The liver increases procoagulant proteins including fibrinogen, platelets can become more reactive and diuresis or dehydration can concentrate the blood. The risk is therefore real but cannot be predicted from urinary antithrombin loss alone. Venous thromboembolism Deep vein thrombosis can cause unilateral leg swelling, pain and warmth. Pulmonary embolism can cause sudden breathlessness, chest pain, coughing blood, rapid heart rate or collapse. Renal vein thrombosis can cause flank pain, haematuria or sudden kidney deterioration, although it can be silent. Risk is highest with severe hypoalbuminaemia and is particularly recognised in membranous nephropathy, but any nephrotic cause can be complicated by thrombosis. Anticoagulation is individualised A confirmed venous thrombosis is treated with anticoagulation unless a major contraindication exists. Preventive anticoagulation is not automatic for everyone with nephrotic syndrome. The nephrologist considers serum albumin, underlying diagnosis, previous thrombosis, immobility, obesity, cancer, pregnancy and planned procedures against bleeding risk. Kidney function affects the choice and dose of anticoagulant. Starting aspirin or anticoagulation without specialist assessment can cause serious harm. Acute kidney injury in nephrotic syndrome Nephrotic syndrome can coexist with normal filtration or with acute kidney injury. Possible mechanisms include low effective circulating volume, sepsis, renal vein thrombosis, drug toxicity and severe glomerular inflammation. Minimal change disease can cause acute kidney injury in adults even without another obvious trigger. Treatment depends on the mechanism. Giving fluid automatically to every swollen person can worsen pulmonary oedema, while excessive diuresis can worsen underfilling. Long term kidney and cardiovascular risk Persistent proteinuria is both a marker and a driver of kidney damage. Filtered proteins activate tubular and interstitial inflammation, contributing to fibrosis and progressive chronic kidney disease. Hypertension, dyslipidaemia, diabetes, smoking and reduced filtration increase cardiovascular risk. Remission or substantial proteinuria reduction is therefore an important treatment goal even when symptoms are mild. General treatment principles Treatment has two connected parts. Supportive care reduces protein leakage, blood pressure, oedema and complications. Cause specific care treats infection, autoimmunity, a plasma cell disorder, cancer or a primary podocyte disease when indicated. The balance depends on diagnosis, disease activity, chronic scarring, age, pregnancy, infection risk and personal preferences. Immunosuppression should not be started solely because urine contains protein and blood. Dietary sodium and fluid Reducing dietary sodium helps control oedema and blood pressure and improves the antiproteinuric effect of renin angiotensin system blockade. Severe salt restriction can reduce appetite and nutrition, so advice should remain practical. Routine fluid restriction is not required for every person. It is used when severe oedema, hyponatraemia or reduced urine output makes free water intake unsafe. A renal dietitian can adapt advice to culture, food access, kidney function and treatment. Diuretics for oedema Loop diuretics such as furosemide are commonly used for nephrotic oedema. Higher doses may be needed because reduced kidney delivery and albumin binding can make response less predictable. A thiazide like diuretic or another tubular diuretic can be added for resistant oedema under close monitoring. Rapid fluid removal can cause dizziness, acute kidney injury, low sodium, low potassium or thrombosis. Daily review is essential during intensive treatment. ACE inhibitors and ARBs ACE inhibitors and angiotensin receptor blockers reduce pressure within glomerular capillaries and lower proteinuria. They are important supportive treatments in many proteinuric kidney diseases, even when blood pressure is not markedly raised. Creatinine and potassium are checked before and after starting or increasing the dose. They may need temporary interruption during severe acute kidney injury, hypotension or hyperkalaemia and are contraindicated during pregnancy. Do not combine ACE inhibitors and ARBs routinely Combining an ACE inhibitor with an ARB may reduce proteinuria further but increases acute kidney injury and hyperkalaemia risk. Routine dual blockade is therefore avoided. A rising creatinine after starting one agent requires assessment of volume, renal artery disease, medicines and the size of the change rather than immediate permanent abandonment. The aim is the highest tolerated evidence based dose with safe monitoring, not maximal dose at any cost. Immunosuppression is diagnosis specific Glucocorticoids, rituximab, cyclophosphamide, mycophenolate and calcineurin inhibitors have different roles across glomerular diseases. The same drug can be lifesaving in one diagnosis and harmful or ineffective in another. Treatment also requires infection prophylaxis, fertility discussion, blood monitoring and cancer risk awareness where relevant. The biopsy and disease specific guideline determine the regimen rather than the label nephrotic or nephritic alone. Treating minimal change disease A typical first episode in a child is usually treated with a defined course of prednisolone under paediatric guidance. Relapses are monitored through urine protein and treated according to frequency and steroid response. Frequently relapsing or steroid dependent disease may require a steroid sparing medicine such as levamisole, mycophenolate, a calcineurin inhibitor, cyclophosphamide or rituximab. Adults usually receive glucocorticoids after biopsy confirmation, with alternatives when steroids are contraindicated or disease frequently relapses. Treating FSGS Primary FSGS with nephrotic syndrome is commonly treated with high dose glucocorticoid or a calcineurin inhibitor under specialist care. Secondary FSGS is managed by treating the driver, reducing proteinuria and controlling blood pressure rather than routine immunosuppression. Genetic FSGS is often steroid resistant and may require genetic counselling and supportive treatment. FSGS can recur after kidney transplantation, especially in some primary forms, which affects transplant planning. Treating membranous nephropathy All patients receive supportive care for proteinuria, blood pressure, oedema and cardiovascular risk. Disease specific immunosuppression is based on risk of progression, proteinuria, kidney function, antibody activity and complications. Options can include rituximab, cyclophosphamide with glucocorticoids or a calcineurin inhibitor. Thrombosis prevention is considered carefully because severe nephrosis and membranous disease increase risk, while anticoagulation also creates bleeding risk. Treating IgA nephropathy Optimised supportive care is central and includes blood pressure control, renin angiotensin system blockade, sodium reduction and appropriate SGLT2 inhibition. Persistent proteinuria despite supportive care identifies greater progression risk. Disease specific options now include selected targeted or immune modifying treatments under current specialist guidance. Rapidly progressive IgA nephropathy with crescentic kidney failure is unusual and is treated differently from stable haematuria with chronic proteinuria. Treating infection related glomerulonephritis Active bacterial infection is treated promptly with appropriate antimicrobials and source control. Blood pressure, oedema, electrolytes and acute kidney injury receive supportive treatment. Immune suppression is not routine because it can worsen infection. Kidney recovery is common in children but can be incomplete in older adults or people with diabetes, severe infection or pre existing kidney disease. Treating lupus nephritis Hydroxychloroquine is recommended for most people with lupus nephritis unless contraindicated. Active proliferative or membranous lupus nephritis usually requires glucocorticoids combined with another immune therapy. Options include mycophenolate, cyclophosphamide and selected add on treatments such as belimumab or a calcineurin pathway medicine. Pregnancy plans, infection, fertility, biopsy class and response influence the regimen and maintenance treatment. Treating ANCA associated glomerulonephritis Organ threatening ANCA associated vasculitis requires rapid induction treatment. Current regimens use glucocorticoids with rituximab or cyclophosphamide. Avacopan can reduce glucocorticoid exposure in selected pathways. Plasma exchange is considered in selected people with very severe kidney failure, diffuse alveolar haemorrhage with hypoxaemia or anti GBM overlap. Maintenance treatment reduces relapse risk after remission and differs according to ANCA type, previous relapse and medicine tolerance. Treating anti GBM disease Anti GBM disease is treated urgently with plasma exchange to remove circulating antibodies. Cyclophosphamide reduces new antibody production and glucocorticoids control inflammation. Plasma exchange continues until antibodies are no longer detectable according to specialist protocols. Kidney recovery is less likely when presentation is late with dialysis dependence and extensive irreversible crescents, but pulmonary haemorrhage still requires aggressive treatment. Dialysis and kidney replacement therapy Severe glomerular disease can require temporary or long term dialysis. Urgent indications include refractory hyperkalaemia, pulmonary oedema, severe acidosis and uraemic complications. Dialysis supports kidney functions but does not treat the underlying immune process. Some people recover enough to stop dialysis after inflammation is controlled, while others progress to permanent kidney failure and transplant assessment. Monitoring response Proteinuria is measured sequentially because reduction predicts improved kidney outcome in many glomerular diseases. Creatinine, eGFR, albumin, blood pressure, weight and urine sediment provide complementary information. Immune markers such as anti GBM antibody, PLA2R antibody or lupus serology can support disease specific monitoring but do not replace clinical assessment. Treatment toxicity monitoring can be as important as disease monitoring. Prognosis varies widely Minimal change disease in children usually has excellent long term kidney survival despite possible relapses. IgA nephropathy can remain mild or progress slowly over decades. ANCA and anti GBM disease can destroy kidney function over days if untreated. FSGS, membranous nephropathy and lupus nephritis have outcomes that depend on remission, chronic scarring and treatment complications. The diagnostic name alone does not determine an individual's future. Trends in proteinuria, filtration and blood pressure provide important prognostic information. Follow up after apparent recovery A normal creatinine does not always mean glomerular disease has resolved because significant proteinuria or microscopic haematuria can persist. Follow up includes urine protein, blood pressure, kidney function and medicine review. Vaccination, bone health, infection risk, fertility and cardiovascular prevention may require ongoing attention after immunosuppression. Long term surveillance also detects recurrence before severe symptoms develop. The central safety message Blood and protein in urine can be the first sign of a glomerular disorder even when you feel well. Rapid kidney decline, severe hypertension or lung bleeding with an active urine sediment is a nephrology emergency. Nephrotic syndrome adds major infection, thrombosis and acute kidney injury risks, especially when albumin is very low. Safe management identifies the cause through targeted testing and often biopsy, treats complications immediately and uses disease specific therapy rather than one treatment for every pattern.

Glomerular disease damages the kidney's filtration barrier and can produce nephritic, nephrotic or overlapping patterns. Rapidly progressive kidney failure, pulmonary haemorrhage and severe hypertension require urgent specialist care, while heavy protein loss also creates major oedema, infection and thrombosis risks.