Compare conditions

Put any two — or three — conditions side by side, adult or pediatric, to spot the look-alike differences fast, row by row.

Acute GN

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In one line

·The glomerulus (kidney filter) is under immune attack, and its leaky barrier is letting blood and protein spill into the urine.

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Normal physiology

·Each glomerulus is a ball of capillaries (tiny blood vessels) wrapped in a basement membrane (a thin protein sheet) and covered by podocytes (specialized cells with finger-like foot processes that interlock to form a tight barrier). Blood flows into the glomerulus under pressure, and water, salts, and small waste molecules are pushed through the filter into Bowman space (a cup-shaped chamber that catches the filtered fluid), which becomes urine. Red blood cells, platelets, and large proteins like albumin are too big to pass through the healthy filter, so they stay in the bloodstream.

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What goes wrong

·The immune system attacks the glomerular filter, punching holes in the barrier and clogging the capillaries with inflammation. This single break explains why red blood cells and protein leak into the urine, why blood pressure climbs, why urine output drops, and why waste backs up in the blood.

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Hallmark signs

·Cola-colored or tea-colored urine (blood in urine you can see)
·Puffy face and swollen ankles (edema)
·New high blood pressure or worsening of existing high blood pressure
·Much less urine than usual (oliguria—less than about 2 cups a day)
·Feeling very tired and generally unwell (malaise)
·Dull ache in the back or sides (flank pain)
·Foamy or bubbly urine
·Coughing up blood (hemoptysis) along with blood in urine (pulmonary-renal syndrome)

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Red flags · escalate now

·Coughing up blood along with blood in urine—warns of pulmonary-renal syndrome; needs urgent kidney biopsy and immune-suppressing drugs to save kidneys and lungs
·Kidney waste number (creatinine) rising fast (more than 0.3 in 48 hours or doubling in a week)—signals rapidly progressive GN; permanent kidney damage can happen in days without treatment
·Very little or no urine output (oliguria or no urine output (anuria))—means acute kidney injury; needs urgent kidney specialist and may need dialysis to clean the blood
·Uremic symptoms (confusion, pericardial rub, seizures)—show life-threatening toxin buildup from kidney failure; emergency dialysis may be needed
·Severe high blood pressure with headache, vision changes, or chest pain—with high blood pressure (hypertensive) emergency damaging brain, eyes, or heart; must lower pressure quickly in hospital

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Workup

·Urinalysis with microscopy
·Serum creatinine and blood urea nitrogen (BUN)
·Complement levels (C3 and C4)
·Anti-streptolysin O (ASO) titer and anti-DNase B
·Antinuclear antibody (ANA) and anti-double-stranded DNA (anti-dsDNA)
·Antineutrophil cytoplasmic antibodies (ANCA): MPO and PR3
·Anti-glomerular basement membrane (anti-GBM) antibody
·Kidney biopsy with immunofluorescence and electron microscopy

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Treatment

·ACE inhibitor (such as lisinopril) or ARB (such as losartan) to control blood pressure and reduce protein leak
·Loop diuretics (such as furosemide) and salt restriction for volume overload
·Corticosteroids (methylprednisolone IV 500–1000 mg daily for 3 days, then oral prednisone 1 mg/kg/day) for immune suppression
·Cyclophosphamide (oral 2 mg/kg/day or IV 0.5–1 g/m² monthly) or rituximab (375 mg/m² weekly for 4 doses or 1 g on days 1 and 15) for severe or rapidly progressive GN
·Plasmapheresis (plasma exchange, typically 7 sessions over 14 days, 60 mL/kg per session) for anti-GBM disease or severe ANCA-associated rapidly progressive GN
·Antibiotics (such as penicillin V 250–500 mg four times daily or amoxicillin 500 mg three times daily for 10 days) if active strep infection is present
·Renal replacement therapy (hemodialysis or peritoneal dialysis) if severe AKI develops

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NCLEX trap

·In acute glomerulonephritis, blood pressure goes up because the kidney's tiny filters (glomeruli) are swollen and clogged, so the kidney panics and squeezes harder to push blood through. Lower the pressure slowly and gently—just enough to prevent a stroke or fluid backing up into the lungs (pulmonary swelling (edema))—but do NOT rush it down to perfect numbers. Dropping pressure too fast can starve the already-hurt kidney of blood and make things worse. The real job is to calm the immune attack damaging the filters; treating pressure alone does not heal the kidney.
·In acute glomerulonephritis with rising creatinine, do NOT give diuretics unless the lungs are filling with fluid (pulmonary swelling (edema)) and the patient cannot breathe. The swelling happens because damaged filters leak protein and the kidney holds onto salt and water—not because there is simply too much fluid that a pill can fix. Diuretics can drop blood pressure and blood flow to kidneys that are already struggling, push creatinine even higher, and speed the patient toward needing dialysis. Only use them when fluid in the lungs is life-threatening.
·Dark cola-colored urine plus high blood pressure and puffiness around the eyes in a child is acute glomerulonephritis until proven otherwise—not a UTI. A UTI causes cloudy, smelly, painful urine with bacteria and white blood cells (pus cells) but no blood cell casts (clumps of red cells shaped like tiny tubes from the kidney). In glomerulonephritis, you see red blood cell casts and dysmorphic red cells (mangled, oddly shaped red cells squeezed through broken filters). Look at the whole picture—urine color, blood pressure, swelling, and what the urine looks like under a microscope—not just the color alone.
·Acute glomerulonephritis can flip from mild to rapidly progressive glomerulonephritis (RPGN—severe, fast kidney damage happening in days) very quickly. Crescents (piles of immune cells crushing the filters from the inside) and pulmonary bleeding (hemorrhage) (bleeding into the lungs from the same antibodies attacking lung blood vessels) can show up suddenly. If creatinine keeps climbing or the patient coughs up blood, get a kidney biopsy urgently. Do NOT wait for the patient to look sick—the labs are already shouting that the kidneys are failing right now.
·Post-streptococcal acute glomerulonephritis (kidney damage after strep throat, caused by immune complexes not active infection) usually gets better on its own with salt restriction and gentle blood pressure control—no steroids needed. Save steroids (like prednisone or IV methylprednisolone) and heavy-duty immune blockers (cyclophosphamide, rituximab) for rapidly progressive glomerulonephritis, anti-GBM disease (Goodpasture syndrome—antibodies attack kidney and lung), ANCA-associated vasculitis (antibodies blowing up small blood vessels), and severe IgA nephropathy with crescents. Match the strength of treatment to the type and speed of kidney damage.
·In acute glomerulonephritis, low urine output (oliguria) (peeing less than 400 mL a day in an adult, or less than 1 mL per kilogram per hour in a child) and rising creatinine mean the filters are badly swollen and barely working. Measure urine output every shift, weigh the patient at the same time every day (same clothes, same scale), and check creatinine daily. If urine stops or creatinine doubles in 24 hours, dialysis may be needed soon. The window between stable and needing emergency dialysis is narrow—close watching catches trouble early.

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