Medicine – Renal Syndromes

Renal disorders commonly present in a limited number of recognisable clinical syndromes. Identifying the syndrome first helps narrow the differential diagnosis before determining the exact underlying disease.

The main renal syndromes include:

Asymptomatic proteinuria.

Nephrotic syndrome.

Nephritic syndrome.

Haematuria.

Acute kidney injury.

Chronic kidney disease.

1. Asymptomatic Proteinuria

Asymptomatic proteinuria means protein is detected in the urine without obvious oedema, haematuria, renal failure, or other major symptoms.

Older teaching sometimes defines this as:

Proteinuria less than 3 g/day.

However, modern practice more often classifies proteinuria by:

Urine albumin-to-creatinine ratio – ACR

or

Protein-to-creatinine ratio – PCR.

2. Why Proteinuria Matters

Persistent proteinuria may be an early sign of:

Glomerular disease.

Diabetic kidney disease.

Hypertensive kidney disease.

Tubulointerstitial disease.

It may also occur transiently during:

Fever.

Exercise.

Acute illness.

Therefore, persistent proteinuria should usually be confirmed with repeat testing.

3. Nephrotic Syndrome

Nephrotic syndrome results from marked increase in glomerular permeability to plasma proteins.

The classic features are:

Heavy proteinuria.

Hypoalbuminaemia.

Oedema.

Hyperlipidaemia.

4. Proteinuria in Nephrotic Syndrome

Older notes often use:

Proteinuria greater than 3 g/day.

The more commonly used adult threshold is approximately:

Greater than 3–3.5 g/day.

In practice, nephrotic-range proteinuria may also be estimated using a:

Urine protein-to-creatinine ratio.

5. Hypoalbuminaemia

Because large amounts of albumin are lost in the urine, serum albumin falls.

A classic nephrotic value is:

Serum albumin below about 25–30 g/L.

The exact threshold varies, but marked hypoalbuminaemia supports the diagnosis.

6. Oedema in Nephrotic Syndrome

Loss of albumin lowers plasma oncotic pressure.

This promotes movement of fluid from the circulation into the tissues, producing:

Peripheral oedema.

Periorbital oedema.

Ascites.

Generalised oedema in severe cases.

7. Hyperlipidaemia

The liver responds to low oncotic pressure by increasing synthesis of:

Lipoproteins.

Therefore nephrotic syndrome is commonly associated with:

Hypercholesterolaemia.

Hypertriglyceridaemia.

8. Lipiduria

Lipid may also appear in the urine.

Urine microscopy can demonstrate:

Oval fat bodies.

These may show a:

Maltese-cross appearance

under polarised light.

9. Causes of Nephrotic Syndrome

Important causes include:

Minimal change disease.

FSGS.

Membranous nephropathy.

Diabetic kidney disease.

Amyloidosis.

SLE.

Infections.

Drugs.

10. Complications of Nephrotic Syndrome

Nephrotic syndrome can lead to important complications.

These include:

Venous thromboembolism.

Infection.

Malnutrition.

Vitamin D loss.

Hypocalcaemia.

Hyperlipidaemia.

11. Why Thrombosis Occurs

Patients lose anticoagulant proteins in the urine, including:

Antithrombin.

At the same time, some procoagulant factors increase.

This creates a:

Hypercoagulable state.

12. Nephritic Syndrome

Nephritic syndrome results from inflammatory injury to the glomeruli.

The classic features include:

Haematuria.

Hypertension.

Oedema.

Oliguria.

Reduced GFR.

Proteinuria, usually less severe than in nephrotic syndrome.

13. Haematuria in Nephritic Syndrome

Haematuria may be:

Microscopic

or

Macroscopic.

Urine may appear:

Tea-coloured

or

Cola-coloured.

This suggests glomerular bleeding.

14. Dysmorphic Red Cells

Glomerular haematuria often produces:

Dysmorphic red blood cells.

These become distorted while passing through a damaged glomerular filtration barrier.

15. Red Blood Cell Casts

A particularly important finding is:

Red blood cell casts.

These strongly suggest:

Glomerulonephritis.

Therefore:

Haematuria + RBC casts + reduced GFR → think nephritic glomerular disease.

16. Hypertension in Nephritic Syndrome

Hypertension develops because impaired filtration leads to:

Sodium retention.

Water retention.

Increased intravascular volume.

This can also contribute to:

Oedema.

17. Oliguria

Oliguria means:

Reduced urine output.

It occurs because inflamed glomeruli filter less plasma.

Severe cases may progress to:

Acute kidney injury.

18. Proteinuria in Nephritic Syndrome

Proteinuria is usually:

Mild to moderate.

However, some diseases can produce a mixed:

Nephritic-nephrotic pattern.

Therefore, heavy proteinuria does not completely exclude inflammatory glomerulonephritis.

19. Causes of Nephritic Syndrome

Important causes include:

Post-infectious glomerulonephritis.

IgA nephropathy.

Lupus nephritis.

ANCA-associated vasculitis.

Anti-GBM disease.

Membranoproliferative GN.

20. Nephrotic versus Nephritic – Note Form

Nephrotic syndrome:

Heavy proteinuria.

Hypoalbuminaemia.

Generalised oedema.

Hyperlipidaemia.

Lipiduria.

Thrombosis risk.

Nephritic syndrome:

Haematuria.

RBC casts.

Hypertension.

Oedema.

Oliguria.

Reduced GFR.

Usually less proteinuria than nephrotic syndrome.

21. Haematuria as a Renal Syndrome

Haematuria means blood in the urine.

It can be:

Microscopic

or

Macroscopic.

22. Microscopic Haematuria

Microscopic haematuria means red blood cells are detected on:

Urine microscopy

or inferred from:

Positive urine dipstick for blood

with confirmation where appropriate.

The urine may look completely normal.

23. Macroscopic Haematuria

Macroscopic haematuria means:

Visible blood in the urine.

The urine may appear:

Pink.

Red.

Brown.

Tea-coloured.

The colour and associated features may help localise the source.

24. Glomerular Haematuria

Features suggesting a glomerular source include:

Dysmorphic RBCs.

RBC casts.

Proteinuria.

Tea- or cola-coloured urine.

Associated renal impairment.

25. Non-Glomerular Haematuria

Features suggesting bleeding from elsewhere in the urinary tract include:

Clots.

Bright red urine.

Relatively normal-shaped RBCs.

Possible causes include:

Stones.

UTI.

Tumours.

Trauma.

26. Glomerulonephritis

Glomerulonephritis is an inflammatory or immune-mediated condition affecting the:

Renal glomeruli.

It can cause:

Haematuria.

Proteinuria.

Reduced GFR.

Hypertension.

Nephritic syndrome.

Nephrotic syndrome in some conditions.

27. Structural Changes in Glomerulonephritis

Possible pathological changes include:

Cellular proliferation.

Leukocyte infiltration.

Immune deposition.

Basement membrane abnormalities.

Crescent formation.

Glomerular sclerosis.

28. Interstitial Nephritis

Interstitial nephritis is an inflammatory disorder involving primarily the:

Renal interstitium

and

Tubules.

This is distinct from glomerulonephritis, which primarily affects:

Glomeruli.

29. Acute Interstitial Nephritis

The acute form commonly presents with:

Acute kidney injury.

Sterile pyuria.

Mild proteinuria.

Microscopic haematuria.

White blood cell casts.

30. Common Causes of Interstitial Nephritis

Important causes include:

Drugs.

Infections.

Autoimmune disease.

Drug-induced disease is especially common.

31. High-Yield Anatomical Distinction

Remember:

Glomerulonephritis → glomeruli.

Interstitial nephritis → interstitium and tubules.

Pyelonephritis → renal interstitium and collecting system, usually due to infection.

32. Acute Kidney Injury as a Renal Syndrome

Although not included in the original list, another major renal syndrome is:

Acute kidney injury – AKI.

AKI is defined by an acute deterioration in renal function, usually detected by:

Rising serum creatinine

and/or

Reduced urine output.

33. Causes of AKI

AKI is commonly divided into:

Pre-renal causes.

Intrinsic renal causes.

Post-renal causes.

34. Pre-Renal AKI

Pre-renal AKI occurs because of reduced renal perfusion.

Examples include:

Hypovolaemia.

Haemorrhage.

Sepsis.

Heart failure.

35. Intrinsic Renal AKI

Intrinsic renal causes include:

Acute tubular injury.

Glomerulonephritis.

Acute interstitial nephritis.

Renal vascular disease.

36. Post-Renal AKI

Post-renal AKI results from:

Urinary tract obstruction.

Examples include:

Prostatic obstruction.

Stones.

Tumours.

Bilateral ureteric obstruction.

37. Chronic Kidney Disease as a Renal Syndrome

Another major presentation is:

Chronic kidney disease – CKD.

CKD refers to persistent abnormalities of kidney structure or function lasting:

At least 3 months.

38. CKD Features

Patients may have:

Reduced eGFR.

Persistent albuminuria.

Hypertension.

Anaemia.

Electrolyte abnormalities.

Mineral and bone disease.

Uraemic symptoms in advanced disease.

39. Renal Syndromes – Note Form

Asymptomatic proteinuria:

Protein detected without major symptoms.

May be early glomerular or systemic renal disease.

Confirm persistence.

Nephrotic syndrome:

Heavy proteinuria.

Hypoalbuminaemia.

Oedema.

Hyperlipidaemia.

Lipiduria.

Nephritic syndrome:

Haematuria.

RBC casts.

Hypertension.

Oedema.

Oliguria.

Reduced GFR.

Haematuria syndrome:

Microscopic or visible haematuria.

Determine whether glomerular or non-glomerular.

AKI:

Rapid deterioration in renal function.

Pre-renal, intrinsic, or post-renal.

CKD:

Persistent kidney abnormality for at least 3 months.

May involve reduced eGFR and/or albuminuria.

40. Important Corrections to the Original Notes

The statement:

“Asymptomatic proteinuria <3 g/day”

is an older simplified definition.

Modern assessment generally uses:

ACR or PCR

and focuses on whether proteinuria is:

Persistent

and whether it reaches:

Nephrotic range.

The statement:

“Nephrotic syndrome = proteinuria >3 g/day”

is broadly correct but modern adult teaching more often uses approximately:

>3–3.5 g/day

or an equivalent spot urine protein measurement.

The original nephrotic definition should also explicitly include:

Hyperlipidaemia

and often:

Lipiduria.

The original nephritic definition is incomplete without:

Reduced GFR

and the high-yield urinary finding:

RBC casts.

Glomerulonephritis and interstitial nephritis should be distinguished anatomically:

GN → GLOMERULI.

INTERSTITIAL NEPHRITIS → INTERSTITIUM + TUBULES.

Key Clinical Pattern

For nephrotic syndrome, think:

PROTEIN LOSS.

HEAVY PROTEINURIA + LOW ALBUMIN + OEDEMA + HIGH CHOLESTEROL.

For nephritic syndrome, think:

GLOMERULAR INFLAMMATION.

HAEMATURIA + RBC CASTS + HYPERTENSION + OLIGURIA + REDUCED GFR.

For anatomical localisation:

GLOMERULONEPHRITIS → GLOMERULI.

INTERSTITIAL NEPHRITIS → INTERSTITIUM AND TUBULES.

A useful overall approach is:

FIRST IDENTIFY THE RENAL SYNDROME → THEN IDENTIFY THE UNDERLYING DISEASE.