Nephrology Revision Guide ✅

🫘 Nephrology is physiology at the bedside. Start with four questions: is kidney function acute or chronic?, is urine normal or abnormal?, is the problem volume/electrolyte/acid-base?, and is there a systemic disease driving renal injury? For exams and ward work, always connect the lab result to function: creatinine/eGFR = filtration, ACR = glomerular leak, potassium = arrhythmia risk, bicarbonate/pH = acid-base handling, and urine output = perfusion/tubular function.

✅ 1. Core Renal Anatomy and Physiology

🧬 1.1 Nephron Basics

• Glomerulus: filters plasma; damage causes haematuria and proteinuria.
• Proximal tubule: reabsorbs most sodium, water, bicarbonate, glucose and amino acids.
• Loop of Henle: creates medullary concentration gradient; loop diuretics act here.
• Distal convoluted tubule: fine-tunes sodium/calcium handling; thiazides act here.
• Collecting duct: responds to aldosterone and ADH; controls potassium, acid secretion and water balance.
• Juxtaglomerular apparatus: regulates renin release and glomerular filtration pressure.

🩸 1.2 What the Kidneys Do

• Excrete urea, creatinine, drugs and toxins.
• Regulate salt, water and blood pressure through RAAS and natriuresis.
• Maintain potassium balance.
• Maintain acid-base balance by bicarbonate handling and hydrogen ion secretion.
• Produce erythropoietin for red cell production.
• Activate vitamin D for calcium/phosphate/bone metabolism.

🧠 Exam pearl: The kidney is not just a “filter”. CKD causes anaemia, bone disease, acidosis, hypertension and cardiovascular risk because endocrine and tubular functions fail as well as filtration.

🧪 2. Renal Investigations

🩸 2.1 Blood Tests

• Creatinine/eGFR: estimate filtration; creatinine is affected by muscle mass, diet, drugs and acute change.
• Urea: rises with renal dysfunction, dehydration, GI bleed, catabolism and high protein load.
• Potassium: urgent if high because of arrhythmia risk.
• Bicarbonate: low in metabolic acidosis, common in advanced CKD or renal tubular acidosis.
• Calcium/phosphate/PTH/vitamin D: assess CKD-mineral bone disorder.
• FBC: anaemia of CKD, infection, haemolysis or systemic disease.
• CRP/ESR/autoimmune tests: useful when vasculitis, lupus or infection is suspected.

🚽 2.2 Urine Tests

• Dipstick blood: haematuria; persistent blood with protein suggests glomerular disease.
• Dipstick protein: albumin/protein leak; quantify with ACR or PCR.
• ACR: albumin:creatinine ratio; important for CKD risk stratification and diabetic kidney disease.
• Urine microscopy: red cell casts suggest glomerulonephritis; muddy brown casts suggest ATN.
• Urine culture: infection; interpret with symptoms and contamination risk.
• Urine sodium/osmolality: helps assess hyponatraemia and volume states.

🩻 2.3 Imaging

• Renal ultrasound checks kidney size, obstruction, hydronephrosis, stones, cysts and chronicity.
• Small echogenic kidneys suggest chronic irreversible disease.
• Large kidneys may occur in diabetes, amyloid, HIV nephropathy, obstruction or polycystic kidney disease.
• CT KUB is useful for suspected renal colic.
• CT angiography/MRA may assess renal artery stenosis in selected cases.
• Renal biopsy is considered when diagnosis will change management, especially glomerulonephritis, nephrotic syndrome or unexplained AKI.

🚨 3. Acute Kidney Injury

AKI is a sudden fall in kidney function, usually detected by rising creatinine, reduced urine output or both. NICE NG148 covers prevention, detection and management of AKI in adults, children and young people.

🔍 3.1 Causes of AKI

🧪 3.2 AKI Assessment

• Review baseline creatinine/eGFR and timing of rise.
• Assess volume status: mucous membranes, JVP, oedema, postural BP, capillary refill, weight and fluid balance.
• Check urine output and catheter patency if catheterised.
• Look for sepsis, bleeding, hypotension, obstruction, nephrotoxins and contrast exposure.
• Urinalysis is essential: blood/protein may indicate glomerulonephritis.
• Renal ultrasound if obstruction is possible or AKI cause is unclear.
• Medication review: ACEi/ARB, NSAIDs, diuretics, metformin, SGLT2 inhibitors, aminoglycosides, vancomycin, contrast, PPIs.

💊 3.3 AKI Management

• Treat the cause: restore perfusion, treat sepsis, stop nephrotoxins, relieve obstruction.
• Optimise fluid balance - give fluids if hypovolaemic, but avoid overload in heart failure/oliguria.
• Monitor U&E, bicarbonate, potassium, phosphate, calcium and urine output.
• Adjust drug doses to current renal function.
• Manage complications: hyperkalaemia, acidosis, pulmonary oedema, uraemic symptoms.
• Refer to renal team if severe AKI, rapidly worsening function, unclear cause, suspected intrinsic renal disease, refractory complications or need for dialysis.

🚨 Safety pearl: AKI plus blood and protein on urine dip is not “just dehydration” until proven otherwise. Think glomerulonephritis or vasculitis and escalate early.

🧱 4. Chronic Kidney Disease

CKD is abnormal kidney structure or function present for more than 3 months, with implications for health. NICE NG203 covers CKD assessment and management, aiming to slow progression and reduce complications and cardiovascular risk.

📉 4.1 CKD Classification

• CKD is staged by eGFR category and albuminuria category.
• Albuminuria is a powerful predictor of renal progression and cardiovascular risk.
• Do not diagnose CKD from one abnormal eGFR alone unless chronicity is known.
• eGFR may underestimate or overestimate true function in extremes of muscle mass.
• Rapidly declining eGFR, heavy proteinuria, haematuria or resistant hypertension suggests need for specialist review.

🧬 4.2 Causes of CKD

• Diabetes mellitus - commonest cause in many settings.
• Hypertension and vascular disease.
• Glomerulonephritis.
• Polycystic kidney disease.
• Reflux nephropathy/chronic pyelonephritis.
• Obstructive uropathy.
• Drug/toxin injury, including NSAIDs and lithium.
• Systemic disease such as SLE, vasculitis, myeloma and amyloidosis.

💊 4.3 CKD Management Principles

• Control blood pressure and reduce albuminuria.
• Use ACE inhibitor or ARB in appropriate albuminuric CKD, with potassium/creatinine monitoring.
• SGLT2 inhibitors may reduce progression and cardiovascular events in selected CKD patients according to current criteria.
• Manage cardiovascular risk: statins, smoking cessation, weight, diabetes and exercise.
• Avoid nephrotoxins and dose-adjust renally cleared medications.
• Monitor complications: anaemia, acidosis, hyperkalaemia, CKD-mineral bone disorder, fluid overload.
• Discuss kidney replacement therapy or conservative kidney management in advanced CKD when appropriate.

🧠 Exam pearl: CKD risk is not just eGFR. A patient with eGFR 55 and ACR 100 may be at higher renal and cardiovascular risk than someone with eGFR 45 and no albuminuria.

🚽 5. Nephritic and Nephrotic Syndromes

🩸 5.1 Nephritic Syndrome

Nephritic syndrome reflects glomerular inflammation causing blood and protein to leak through the filtration barrier. It can progress rapidly and needs urgent recognition.

• Features: haematuria, proteinuria, hypertension, oedema, reduced eGFR, oliguria.
• Urine: dysmorphic red cells and red cell casts suggest glomerular bleeding.
• Causes: IgA nephropathy, post-infectious GN, lupus nephritis, ANCA vasculitis, anti-GBM disease, membranoproliferative GN.
• Red flags: rapidly rising creatinine, pulmonary haemorrhage, systemic vasculitis symptoms, heavy proteinuria.
• Investigations: urine ACR/PCR, renal profile, complements, ANA/dsDNA, ANCA, anti-GBM, hepatitis/HIV, renal ultrasound, biopsy if indicated.

💧 5.2 Nephrotic Syndrome

Nephrotic syndrome is heavy proteinuria causing hypoalbuminaemia, oedema and hyperlipidaemia. Loss of anticoagulant proteins also increases thrombosis risk.

• Features: oedema, frothy urine, heavy proteinuria, low albumin, high cholesterol.
• Complications: infection, venous thromboembolism, AKI, malnutrition, hypothyroidism due to binding protein loss.
• Causes in children: minimal change disease.
• Causes in adults: membranous nephropathy, FSGS, diabetic kidney disease, amyloidosis, minimal change disease.
• Management: salt restriction, diuretics, ACEi/ARB if appropriate, statin, thrombosis risk assessment, treat cause.

🧂 6. Electrolyte Disorders

🍌 6.1 Hyperkalaemia

• Hyperkalaemia is dangerous because it can cause fatal arrhythmias.
• Causes: AKI, CKD, ACEi/ARB/MRA, potassium supplements, trimethoprim, acidosis, DKA, rhabdomyolysis, haemolysis, adrenal insufficiency.
• Always check for pseudohyperkalaemia from haemolysed sample, thrombocytosis or leukocytosis if clinically inconsistent.
• ECG changes: peaked T waves, PR prolongation, QRS widening, sine-wave pattern, bradyarrhythmia or VF.
• Emergency treatment principles: protect the heart with IV calcium if ECG changes/severe; shift potassium intracellularly with insulin-glucose ± salbutamol; remove potassium with binders/diuretics/dialysis; stop contributors.
• UK Kidney Association guidance provides adult acute hyperkalaemia recommendations and is due for review in 2026.

⬇️ 6.2 Hypokalaemia

• Causes: diuretics, vomiting, diarrhoea, insulin, beta-agonists, hyperaldosteronism, renal tubular disorders, low magnesium.
• Symptoms: weakness, cramps, constipation, ileus, arrhythmias.
• ECG: flattened T waves, ST depression, U waves, prolonged QU interval.
• Check magnesium because hypomagnesaemia makes hypokalaemia hard to correct.
• Replace carefully; IV potassium requires appropriate rate, dilution and monitoring.

💧 6.3 Hyponatraemia

• Hyponatraemia is low sodium relative to water, not simply “salt deficiency”.
• Assess symptoms, speed of onset and volume status.
• Severe symptoms: seizures, coma, severe confusion, reduced consciousness - medical emergency.
• Causes: hypovolaemia, SIADH, heart failure, cirrhosis, nephrotic syndrome, adrenal insufficiency, thiazides, polydipsia.
• Investigations: serum osmolality, urine osmolality, urine sodium, glucose, cortisol, TFTs where appropriate.
• Correction must be controlled to avoid osmotic demyelination.

🧂 6.4 Hypernatraemia

• Usually reflects water deficit, especially in patients unable to drink.
• Causes: dehydration, osmotic diuresis, diabetes insipidus, fever, diarrhoea, excessive sodium administration.
• Symptoms: thirst, confusion, irritability, seizures, coma.
• Correct gradually unless acute and severe; rapid correction can cause cerebral oedema.

⚠️ Electrolyte pearl: Potassium emergencies kill via the heart; sodium emergencies kill via the brain. Potassium management prioritises ECG/cardiac stabilisation, while sodium management prioritises safe correction speed.

🧪 7. Acid-Base Disorders

🧠 7.1 Interpreting Blood Gases

• Step 1: check pH - acidaemia or alkalaemia?
• Step 2: check CO₂ - respiratory contribution.
• Step 3: check bicarbonate/base excess - metabolic contribution.
• Step 4: check compensation - appropriate or mixed disorder?
• Step 5: calculate anion gap if metabolic acidosis.

🧯 7.2 Metabolic Acidosis in Renal Disease

• AKI/CKD reduce acid excretion and bicarbonate regeneration.
• High anion gap acidosis may occur in uraemia, lactic acidosis, DKA or toxins.
• Normal anion gap acidosis occurs in diarrhoea and renal tubular acidosis.
• Severe acidosis can cause hyperkalaemia, reduced cardiac contractility and vasodilation.
• Treat the cause; bicarbonate or dialysis may be needed in severe/refractory cases.

💧 8. Fluid Balance and Oedema

🧃 8.1 Assessing Volume Status

• Hypovolaemia: thirst, dry mucosa, tachycardia, postural hypotension, low JVP, poor skin turgor, low urine output.
• Hypervolaemia: oedema, raised JVP, crackles, hypertension, ascites, weight gain.
• Fluid status is often difficult; use trends in weight, urine output, BP, JVP, creatinine and symptoms.
• Older/frail patients can be simultaneously oedematous and intravascularly depleted.

💊 8.2 Diuretics

• Loop diuretics inhibit sodium-potassium-chloride transport in the loop of Henle; useful for oedema and pulmonary congestion.
• Thiazide-like diuretics act in the distal tubule; useful in hypertension and mild fluid overload.
• Potassium-sparing diuretics include spironolactone, eplerenone, amiloride; monitor potassium and renal function.
• Diuretic resistance can occur in CKD, nephrotic syndrome and heart failure; consider sodium intake, absorption, dosing and combination therapy.

🧊 8.3 Oedema Causes

🧫 9. Urinary Tract Infection and Pyelonephritis

• Lower UTI: dysuria, frequency, urgency, suprapubic pain, cloudy/odorous urine.
• Pyelonephritis: fever, flank pain, rigors, nausea/vomiting, systemic illness.
• Complicated UTI: male sex, pregnancy, catheter, obstruction, renal tract abnormality, immunosuppression or sepsis.
• Send urine culture in recurrent, complicated, pyelonephritis, pregnancy, treatment failure or catheter-associated infection.
• Consider obstruction/infected stone if sepsis plus flank pain or hydronephrosis - urgent urology.
• Asymptomatic bacteriuria is usually not treated except in pregnancy or before some urological procedures.

🧱 9.1 Renal and Perinephric Abscess

• Consider if persistent fever despite antibiotics, flank pain, diabetes, obstruction or stones.
• CT imaging may be needed.
• Management often requires prolonged antibiotics ± drainage.

🪨 10. Renal Stones

• Renal colic: severe colicky loin-to-groin pain, haematuria, restlessness, nausea/vomiting.
• CT KUB is highly sensitive for stones and alternative diagnoses.
• Analgesia: NSAID if safe, antiemetic, fluids if dehydrated but forced fluids do not push stones out.
• Urgent urology if infected obstructed kidney, solitary kidney, AKI, uncontrolled pain, bilateral obstruction or large stone.
• Stone types: calcium oxalate most common, calcium phosphate, uric acid, struvite, cystine.
• Prevention: adequate fluid intake, dietary advice, treat metabolic causes and analyse stone if available.

🚨 Exam pearl: Fever plus obstructing stone is not “just renal colic” - it is an infected obstructed system and needs urgent decompression.

🧬 11. Systemic Renal Disease

🦋 11.1 Lupus Nephritis

• SLE can cause glomerular inflammation ranging from mild urinary abnormalities to rapidly progressive renal failure.
• Look for proteinuria, haematuria, casts, rising creatinine, hypertension and low complement.
• Anti-dsDNA and complement levels can help monitor activity.
• Renal biopsy guides class and treatment.
• Treatment is specialist-led with immunosuppression and renal protection.

🩸 11.2 ANCA Vasculitis and Anti-GBM Disease

• ANCA vasculitis can cause rapidly progressive glomerulonephritis, pulmonary haemorrhage, ENT disease, neuropathy and systemic symptoms.
• Anti-GBM disease can cause pulmonary-renal syndrome with haemoptysis and rapidly progressive renal failure.
• Urine dip often shows blood and protein; creatinine may rise quickly.
• Requires urgent renal/rheumatology care, biopsy and immunosuppression ± plasma exchange in selected cases.

🦴 11.3 Myeloma Kidney

• Light chains can cause cast nephropathy, Fanconi syndrome or amyloidosis.
• Think myeloma in AKI/CKD with anaemia, bone pain, hypercalcaemia, high total protein or recurrent infections.
• Tests: serum free light chains, serum/urine electrophoresis, calcium, FBC, imaging and haematology input.

🧱 12. Polycystic Kidney Disease

• Autosomal dominant polycystic kidney disease causes bilateral renal cysts and progressive CKD.
• Features: hypertension, flank pain, haematuria, UTIs, stones, palpable kidneys.
• Extra-renal: liver cysts, intracranial aneurysms, mitral valve prolapse, hernias.
• Family history is common but de novo mutations occur.
• Management: BP control, CKD monitoring, treat complications, genetic/family counselling, specialist assessment for disease-modifying therapy in selected patients.

🩸 13. Hypertension and the Kidney

• The kidney both causes and suffers from hypertension.
• CKD causes sodium retention, RAAS activation and vascular stiffness.
• Hypertension accelerates nephron loss and increases cardiovascular risk.
• Renovascular disease should be considered in sudden severe/resistant hypertension, flash pulmonary oedema, asymmetric kidneys or creatinine rise after ACEi/ARB.
• Primary hyperaldosteronism should be considered in resistant hypertension or hypertension with hypokalaemia.
• BP targets depend on CKD stage, albuminuria, diabetes, age, frailty and guideline context.

📌 Clinical reasoning: ACE inhibitors and ARBs can cause a small expected creatinine rise because they reduce intraglomerular pressure. A large rise, severe hyperkalaemia or bilateral renal artery stenosis changes the risk-benefit balance.

🦴 14. CKD Complications

🩸 14.1 Anaemia of CKD

• Caused mainly by reduced erythropoietin production and functional iron deficiency.
• Usually becomes more likely as eGFR falls, especially below 30 ml/min/1.73m².
• Assess iron studies, B12, folate, inflammation and blood loss before attributing anaemia to CKD alone.
• Management may include iron replacement and erythropoiesis-stimulating agents under renal guidance.

🦴 14.2 CKD-Mineral Bone Disorder

• Reduced phosphate excretion and vitamin D activation cause secondary hyperparathyroidism.
• Consequences: bone pain, fractures, vascular calcification, itch and abnormal calcium/phosphate balance.
• Monitor calcium, phosphate, PTH, vitamin D and alkaline phosphatase depending on CKD stage.
• Management: dietary phosphate advice, phosphate binders, vitamin D analogues/calcimimetics in selected patients.

🧪 14.3 Uraemia

• Features: nausea, anorexia, pruritus, fatigue, confusion, restless legs, pericarditis, platelet dysfunction.
• Uraemic pericarditis is an indication for urgent dialysis discussion.
• Symptoms matter: dialysis decisions are not based on eGFR alone.

🔄 15. Dialysis and Kidney Replacement Therapy

🩸 15.1 Haemodialysis

• Blood is filtered through a dialyser to remove solutes and fluid.
• Access: arteriovenous fistula preferred for long-term use, graft or dialysis catheter if needed.
• Complications: hypotension, cramps, access infection/thrombosis, disequilibrium syndrome, line sepsis.
• Patients often dialyse several times weekly, but schedules vary.

💧 15.2 Peritoneal Dialysis

• Uses peritoneal membrane as dialysis surface; dialysate is infused into abdomen.
• Can offer independence and home-based therapy.
• Complications: peritonitis, catheter problems, hernias, inadequate clearance, glucose load.
• Cloudy dialysate or abdominal pain in PD is peritonitis until proven otherwise.

🚨 15.3 Indications for Urgent Dialysis

🎁 16. Kidney Transplantation

• Kidney transplant offers better survival and quality of life than long-term dialysis for suitable patients.
• Donors may be living or deceased.
• Immunosuppression commonly includes tacrolimus/ciclosporin, mycophenolate/azathioprine and steroids, but regimens vary.
• Complications: rejection, infection, malignancy, cardiovascular disease, drug toxicity, recurrent original disease.
• Acute graft dysfunction requires urgent assessment: rejection, obstruction, vascular problem, infection, drug toxicity and dehydration must be considered.
• Transplant patients with fever can deteriorate quickly because immunosuppression blunts normal inflammatory responses.

🚨 17. Nephrology Emergencies

📚 18. OSCE / Exam Pearls

• AKI is pre-renal, intrinsic or post-renal until proven otherwise.
• Always dip the urine in AKI.
• Blood plus protein on urine dip suggests glomerular disease.
• New severe hyperkalaemia needs ECG immediately.
• Severe hyperkalaemia treatment has three aims: protect heart, shift potassium, remove potassium.
• Nephrotic syndrome increases thrombosis and infection risk.
• Fever plus obstructing stone is a urological emergency.
• CKD staging needs both eGFR and ACR.
• Small kidneys on ultrasound suggest chronic disease.
• Dialysis is for complications and symptoms, not a single eGFR number alone.

📌 19. Quick Differentials Table

📚 References

• NICE. Chronic kidney disease: assessment and management. NG203.
• NICE. Acute kidney injury: prevention, detection and management. NG148.
• NICE/British National Formulary. Hyperkalaemia treatment summaries.
• UK Kidney Association. Treatment of acute hyperkalaemia in adults guideline, 2023.
• UK Kidney Association guidance should be checked for dialysis, transplantation, CKD complications and specialist renal pathways.

⚠️ Disclaimer

This article is for medical education and exam revision. Clinical decisions should follow current local guidelines, renal referral pathways, electrolyte protocols, antimicrobial policies, dialysis unit procedures, formularies, senior advice and national guidance. Nephrology emergencies such as severe hyperkalaemia, rapidly progressive glomerulonephritis, infected obstruction, severe hyponatraemia, pulmonary oedema with AKI and dialysis access sepsis require urgent senior input.