renal failure and potassium

pathways for clinical learning

Renal Failure

Mark Hall

Clinical Teaching Fellow


Objectives• Revise renal physiology

• Understand nephrotic and nephritic syndromes

• Revise the symptoms of acute kidney injury

• Revise the signs of acute kidney injury

• Revise the investigation and treatment of acute kidney injury


Renal physiology


ureter

cortex

medulla


efferent arteriole

thin descending limb of the loop

of Henle

thick descending limb of the loop of

Henle

distal tubule

collecting duct

afferent arteriole

vein

glomerulus

proximal tubule


What do kidneys do?• Excretion of uremic toxins• Na+/H20 homeostasis• K+ Homeostasis• H+ Homeostasis• Produce humoral agents

– Erythropoietin– Active metabolites of vitamin D– Renin

• BP control


Glomerular Function• GFR – efficiency of the kidney in waste product

disposal• Inversely proportional to creatinine

– Creatinine passively excreted– From skeletal muscle bulk

• Calculated by – (Urine creatinine x Urine flow)/Plasma creatinine

• Estimated Creatinine Clearance– (140-age x mass)/serum creatinine


What happens where?• Glomerulus

– Excretion– Conservation of normal blood products– Hormone control/BP control

• Tubules– Concentrating via osmotic gradient and

counter-current mechanism and collecting duct via ADH


What happens where• Tubules

– Acid Base control in distal and proximal tubules, renal failure = retention of acids

– K+/H+ for Na+ failure = hyperkalaemia


Proteinuria• If glomerular function is disturbed• Occasionally if tubular function is disturbed

Glomerulonephritis Tubular disease

Amount of proteinuria + to ++++ + to ++

Nephrotic syndrome 0 to ++++ No

Dipstick Positive Yes No

K or lambda free chains No Yes


Acute Kidney Injury


Why do kidneys fail?• Pre-renal

– blood supply

• Renal– Glomerulonephritis– Acute tubular necrosis– Interstitial nephritis

• Post-renal– Ureteric obstruction– Urethral obstruction


Acute Kidney Injury• Rapid fall in glomerular filtration rate

• Leading to:– Abrupt rise in urea and creatinine– Fluid volume overload– Oligouria – Hyperkalaemia– Metabolic acidosis


CausesPre-Renal

– Usually in the critically ill patient– < 70mmHg – renal autoregulation impaired

• Hypovolaemia – Haemorrhage, D and V

• Cardiogenic shock• Sepsis• Hepatorenal syndrome

– Usually causes ATN • Recovers over 2 – 3 weeks


CausesIntrinsic Renal

Intrinsic means damage to the glomerulus, renal tubules or interstitium

– Glomerulonephritis– Acute Tubular Necrosis

• Toxic or Ischaemia

– Acute Interstitial Nephritis• Infection or allergic drug reaction


CausesPost Renal

• Usually revealed on renal US

• Ureteric obstruction– Hydronephrosis (usually unilateral)

• Urethral obstruction– Urinary retention– Hydronephrosis (usually bilateral)


Symptoms• May be none

• Frank haematuria

• Proteinuria (frothy urine)

• Oliguria/anuria

• Lower urinary tract symptoms

• Uraemic syndrome


Uraemic syndrome• Neuro

– Fatigue, malaise, depression, cognitive impairment– Involuntary movements, fits, coma– Paraesthesia

• Cardiopulmonary– Dyspnoea– Kussmaul breathing– Pleuritic chest pain

• Skin– Pruritis– Purpura, pallor, pigmentation

• GI– Anorexia, nausea, vomiting– Diarrhoea, constipation, colitis– GI bleeding

• Haem– Anaemia– Bleeding


Signs

• Likely to reflect the cause in AKI

• Assess fluid balance

• Look for effects of hyperkalaemia


When to dialyse acutely• Persistent K+ > 6.0 mmol/L

• Acidosis pH <7.2

• Pulmonary oedema and unable to obtain diuresis

• Pericarditis with tamponade– Relieve tamponade first


Glomerular Disease• Non proliferative (no increase in cells)

– Causes Nephrotic Syndrome

• Proliferative (increase in cells)– Causes Nephritic Syndrome


Nephrotic Syndrome• Proteinuria

– >3.5g/24 hrs• Hypoalbuminaemia

– <30 g/L• Oedema

– Leaky capillaries– Lose protein

• Increased cholesterol

damage occurs to podocytes


Causes of nephrotic syndrome• Glomerular Disease

– Commonly glomerulonephritis• Minimal change glomerulonephritis

– No change on light microscopy, fusion of podocytes– 1st line Steroids 2nd Line Cytotoxic

• Focal segmental glomerulosclerosis– Sclerosis/fibrosis of glomeruli – HIV, Heroin, Diabetes Melitus

• Membranous glomerulonephritis– Thickened basement membrane


History Taking - Symptoms of nephrotic syndrome

• Frothy urine• Effects of hypoalbuminaemia• Drugs• Allergies• Symptoms of vasculitis• Symptoms of malignancy• Chronic or recurrent infections• Symptoms of chronic inflammation


Signs of nephrotic syndrome• Facial swelling

• Xanthelasma

• Xanthomata

• Hypertension

• Pleural effusions

• Ascites

• Peripheral oedema


Complications• Thromboembolism

– ↑ procoagulant factors– ↓anticoagulant factors– Abnormal platelet function– Altered endothelial function– ↓fibrinolytic activity– Intravascular volume depletion

• Renal vein thrombosis• DVT/PE


Complications• Susceptibility to infection

– ↓ serum IgG– ↓ complement activity– Immunisation to pneumococcus

• Hyperlipidaemia


Investigations• FBC, Coag screen

• U&E, LFT, bone profile, lipid profile, glucose

• CRP

• Urine– Dipstick– Spot urine:creatinine ratio– 24 hour urine collection– Bence Jones protein


Investigations• Microbiology

– Hep B/C/HIV– Urine culture (and blood cultures if febrile)

• Immunology– ANA, dsDNA, C3 and C4 levels, serum Igs

and electrophoresis

• Radiology– Renal ultrasound– CXR


Treatment• Treat the cause• Salt restricted diet (<100 mmol/day)• Fluid restriction• May need diuretics (be cautious)• ACEi/A2RB• Consider anticoagulation when albumin

<20 g/L• Treat persistent hyperlipidaemia


Proliferative Glumerular Disease

• Acute renal illness

• Haematuria and Mild Proteinuria – insufficient to cause a decrease in albumin

• Inability to excrete fluids so sodium and water retention

• Decreased GFR – uraemia


Causes• Primary post-infectious

– Bacterial• Streptococci – group A beta-haemolytic strep• Typhoid

– Viral• CMV• Hepatitis• EBV

– Parasitic• Plasmodium falciparum


Causes• Secondary

– SLE– IgA nephropathy– Wegener’s granulomatosis– HSP– Haemoltyic uraemic syndrome


Treatment• Treat the cause

• Treat any consequences of renal impairment


When to dialyse acutely• Persistent K+ > 6.0 mmol/L

• Acidosis pH <7.2

• Pulmonary oedema and unable to obtain diuresis

• Pericarditis with tamponade– Relieve tamponade first


Investigations• Urinalysis

– dipstick, microscopy (casts, crystals)

• Biochemistry– Urea, creatinine, K+,Na+,Ca++,PO4-– Blood gas analysis and serum bicarbonate– CK, myoglobinuria– CRP– Serum immunoglobulins– Protein electrophoresis. BJP in urine


Investigations• Haematology

– FBC, blood film– Coagulation

• Immunology– ANA; dsDNA– ANCA– Complement levels– Anti-GBM– ASO titre


Investigations• Virology

– Hepatitis B,C & HIV

• Radiology– Renal US


Treatment• Correct pre and post renal factors• Optimise cardiac output/renal blood flow• Treat cause• Review medications• Optimise fluid balance; daily weight• Identify and treat complications• Nutritional support• Consider dialysis


Questions?


Summary• Revised renal physiology• Understood nephrotic and nephritic syndromes• Revised the symptoms of acute kidney injury• Revised the signs of acute kidney injury• Revised the investigation and treatment of

acute kidney injury• Revised the common causes, investigation and

treatment of:– Hypokalaemia– Hyperkalaemia

renal failure and potassium

Education