Renal Flashcards
What are diabetics annually screened for?
Microalbuminuria + urine dip at every appointment
Complications of renal replacement therapy
CVD- MI and stroke Malnutrition Renal bone disease Infection Malignancy
Cardiac complications in hyperkalaemia
ECG changes:
Tall tented T waves, broad QRS, prolonged PR, flat P wave
Arrhythmias:
Asystole, VF
Causes of hypercalcaemia
Hyperparathyroidism Thiazide diuretics Malignant disease Sarcoidosis Thyrotoxicosis Vit D intoxication Cortisol deficiency Familial hypocalciuric hypercalcaemia Acidosis
Pathophysiology of CKD
Primary kidney injury:
Diabetes, glomerulonephritis, HTN/reno-vascular disease, pyelonephritis and reflux nephropathy
Nephron loss
Hyperfiltration and hypertrophy of residual nephrons (compensating to maintain GFR), increased glomerular capillary pressure
Sclerosis of hyper-filtering nephrons
Nephrotoxins, decreased perfusion (dehydration, shock), proteinuria, hyperlipidaemia, hyperphospatemia, smoking
Define CKD
Sustained, irreversible decrease in GFR <60ml/min/1.73, for >3months Equations to calculate OR Persistent haematuria/proteinuria/structural abnormalities of the kidneys
Define hypocalcaemia
<2.1mmol/L
Indications for dialysis in CKD
Metabolic acidosis
Hyperkalaemia after 3x rounds of treatment
Anuria/uraemia
BLAST drugs
Define end stage renal disease
<15 GFR
Need for renal replacement therapy
Nephritic syndrome
Haematuria
Oliguria
Proetinuria
Fluid retention
Most common cause of glomerular pathology and CKD?
Diabetic nephropathy
Risk factors for pyelonephritis
Female
Structural urological abnormalities
Diabetes
Presentation of pyeloneprhitis
High fever and rigors
Loin to groin pain
Dysuria and urinary frequency
Haematuria
Other non-specific symptoms (e.g. vomiting)
Pain on bimanual palpation of renal angle
Investigations of CKD
Determine aetiology
Evaluate complications
Bloods (FBC, ESR, U&E, glucose, low Ca, high phosphate, high ALP, high PTH)
Urine (dip, MC&S, albumin:creatinine ratio)
USS kidney (small in CKD) and bladder (obstruction)
Biopsy
3 types of fluid replacement
5% glucose:
Method for administering IV water, not bulk blood volume
Only 5% stays in IV space
Distribution as for water
0.9% saline:
Better for resuscitating blood volume
33% stays in IV space
Distribution as for ECF
Colloid:
5% human albumin
Best for resuscitating blood volume in very haemodynamically compromised patient
Metabolic alkalosis characteristics on ABG
↑ pH
↑ HCO3-
↑ BE
Causes of metabolic alkalosis
Gastrointestinal loss of H+ ions (e.g. vomiting, diarrhoea)
Renal loss of H+ ions (e.g. loop and thiazide diuretics, heart failure, nephrotic syndrome, cirrhosis, Conn’s syndrome)
Iatrogenic (e.g. addition of excess alkali such as milk-alkali syndrome)
Presentation of CKD at different stages
1-3
Frequently asymptomatic
Via screening of at risk pts
4-5
Endocrine/metabolic/water/electrolyte disturbances
Prevention of diabetic nephropathy
Blood pressure control
Glycaemic control
CVS risk control (stop smoking, reduce cholesterol, consider aspirin)
Define hypercalcaemia
> 2.6mmol/L corrected calcium
> 3mmol/L severe
2 mechanisms, their effects and their management of lack of 1,25 vitamin D production in CKD
Hypocalaemia:
Causes bone pain
Managed with vit D and calcium supplementation
Raised PTH:
Causes fractures, osteomalacia, ostetitis fibrosa
Managed by phosphate binders, vit D/analogues, calcimimetics, 1-alpha calcitol
Management of UTI
Trimethoprim/nitrofurantoin
3 days:
For simple lower urinary tract infection in women
5-10 days:
For women that are immunosuppressed, have abnormal anatomy or impaired kidney function
7 days:
For men, pregnant women or catheter-related
Presentation of lower UTI
Dysuria (pain, stinging or burning when passing urine)
Suprapubic pain or discomfort
Frequency
Urgency
Incontinence
Confusion commonly the only symptom in older/frail patients
Bacterial causes of UTI
E. coli Klebsiella pneumoniae Enterococcus Pseudomonas aeruginosa Staph saprophyticus Candida albicans (fungal)
Metabolic acidosis characteristics on ABG
↓ pH
↓ HCO3-
↓ BE
Causes of metabolic acidosis
Increased acid production or acid ingestion
Decreased acid excretion or rate of gastrointestinal and renal HCO3– loss
Define nephritis
Inflammation of the kidneys
Non-specific and not a diagnosis
Progression of diabetic nephropathy
GFR elevated (glomerular and tubular hypertrophy) Glomerular hyperfiltration (mesangial expansion due to ongoing damage) Microalbuminuria (30-300mg albumin/24hrs) - early warning of renal problems and risk factor for CKD
Causes of hypertension
Essential (95%) - no identifiable cause Secondary (5%) Chronic renal disease Coartication of aorta Endocrine disease (Cushings, conns, phaeochromocytoma, acromegaly Raised ICP Pre-eclampsia Drugs (steroids, COCP, NSAIDs)
Causes of hypokalaemia
Excessive renal loss:
Drugs (thiazides, loop)
Endocrine (aldosterone excess)
Inherited defects
Magnesium deficiency (Na/K/ATPase)
Process driving K+ into cells:
Acute alkalosis
Insulin
Thyrotoxicosis
GI losses:
Diarrhoea
Vomiting
Low dietary K
Cardiac complications in hypercalcaemia
ECG changes:
Short QT
Arrythmias uncommon
Causes of hypocalcaemia
Alkalosis Hypoparathyroidism Renal failure Vit D deficiency Malabsorption Acute pancreatitis Rhabdomyolsis Sepsis Low Mg
Causes of hyponatraemia
Excess intake/water retention:
SIADH, drugs, CCF, cirrhosis, CKD/nephrotic syndrome, hypothyroidism, pregnancy
Renal Na loss:
Diuretics, mineralocorticoid deficiency, tubular disorders, SIADH, cerebral salt wasting
Other Na loss:
Vomiting, diarrhoea, burns
Pseudo-hyponatraemia:
Hyperproteinaemia, hyperlipidaemia
Define glomerulonephritis
Umbrella term applied to conditions causing inflammation of or around the glomerulus
Causes of UTI
Bacteria from faeces
Spread through sexual activity
Incontinence/hygiene issues
Urinary catheters
Management of 3 mechanisms of abnormal kidney excretion in CKD
Fluid retention:
Leads to HTN
Managed by salt and fluid restriction, loop diuretics
Potassium retention:
Leads to hyperkalaemia (muscle weakness, arrhythmias)
Managed with low K diets, correction of acidosis
Acid retention:
Caused by metabolic acidosis
Managed by sodium bicarbonate therapy
Management of CKD
Identify and treat reversible causes (relieve obstruction, avoid nephrotoxins)
Delay or halt progression of CKD (BP management)
Manage CVD risk (lifestyle, BP, lipid and glycaemic control)
Diagnose and treat pathologic manifestations of CKD (anaemia, mineral and bone disorders, treat acidosis and oedema, restless legs and cramps)
Causes of hyperkalaemia
Reduced renal loss: Low GFR K-sparing diuretics Trimethoprim RAAS inhibiting drugs ACE inhibitors Addisons Dietary excess
K+ release from cells: Acidosis Tumour lysis Insulin deficiency Depolarising muscle paralysis
Definition and stages of hypertension
Raised blood pressure in the systemic vascular bed >140/90mmHg
Normal <120/<80
Pre-HTN 120-139/80-89
Stage 1 40-159/90-99
Stage 2 >160/>100
Define hyponatraemia
<135mmol/L sodium
Clinical consequences at <125mmol/L
Define pyelonephritis
Infection in the renal pelvis
Treatment of hypernatraemia
Stop water loss (antiemetic, stop diuretic, treat diarrhoea)
Aim to replace water (orally or 5% glucose)
Define hyperkalaemia
> 4.7mmol/L
Clinical consequences >6moml/L
Urethral syndrome
Lower urinary tract syndromes: Urinary frequency Urgency Dysuria Suprapubic discomfort
With no recognised urinary pathogen/abnormality
Define hypokalaemia
<3.5mmol/L potassium
Renal consequences of hypertension
hypertensive renal disease
Hyaline arteriosclerosis in renal arterioles
Chronic and progressive renal ischaemia
Tubular atrophy, intestinal fibrosis and progressive glomerular sclerosis
Progressive CKD (small atrophied and fibrosed kidneys)
Vicious cycle of worsening HTN and CKD
Causes of hypernatraemia
Water loss Blunted thirst with age Diabetes insipidus Diabetes mellitus Diuretic use Iatrogenic (excess saline)
ADH
Where does it act?
What does it do?
What increases/decreases secretion?
Acts on renal collecting ducts
Increases permeability to water (aquaporin channels) to increase water absorption
Raised secretion: Increase in plasma osmolality, Pain, stress, nausea Drugs Lung and CNS lesions Ectopic pregnancy Decreased plasma volume
Decreased secretion:
Decrease in plasma osmolality
Increase in plasma volume
Ethanol
Mechanism of metabolic alkalosis
Decreased hydrogen ion concentration
Leading to increased bicarbonate
Alternatively a direct result of increased bicarbonate concentrations
What is CKD associated with?
HTN Anaemia Mineral and bone disorders CVS complications More common >65
Define cystitis
Inflammation of the bladder
Normally caused by UTIs
Mechanism, effect and management of lack of erythropoietin production in CKD
Mechanism: Anaemia
Effect: Tiredness, LVH
Management: Epoetin, iron and ferritin collection
UTI in pregnancy increases risk of
Pyelonephritis
Premature rupture of membranes
Pre-term labour
Signs and symptoms of uraemia
CNS:
Encephalopathy, fits, twitch or tremor, tiredness
Peripheral neuropathy
GI:
Anorexia (loss of appetite & weight), N&V, colitis, metallic taste, halitosis
Resp:
Pleuritis, pleural effusion
Cardio:
Pericarditis
Endocrine:
Growth retardation, sexual dysfunction
Skin:
Pruritus, “half-and-half” nails
Pro-haemorrhagic uraemia - impaired platelet function
Effects of CKD on CVS health
RAAS activation:
Leads to LVH
Managed by ACE inhibitors, angiotensin receptor blockers,
Microinflammation and HTN:
Lead to CAD, CHF, arrhythmias
Managed by BP control <130/80
Investigations of UTI
Urine dip:
Nitrites
Leukocytes
Investigations for pyelonephritis
Urine dip:
Bood, protein, leukocyte esterase, nitrite
CT
USS
DMSA scan (recurrent pyelonephritis)
Management of diabetic nephropathy
Optimising blood glucose levels and BP
ACE inhibitors (even if BP normal)
Cardiac complications in hypocalcaemia
ECG changes:
Long QT
Arrhythmias:
VT, heart block
Nephrotic syndrome
Peripheral oedema
Proteinuria
Serum albumin (<25g)
Hypercholesterolaemia
Chronic pyelonephritis
Recurrent kidney infections
Leads to scarring of the renal parenchyma
Can result in chronic kidney disease
Can result in abscess and/or pus in or around the kidney
May be a role for prophylactic antibiotics
Management of pyelonephritis
Blood and urinary cultures
Broad spectrum antibiotics (e.g. co-amoxiclav) until culture and sensitivities are available
Admission if systemically unwell or complicated
IV rehydration
Analgesia
Antipyretics
Cardiac complications in hypokalaemia
ECG changes:
ST depression, flat T waves, U wave, extra systoles
Arrhythmias:
AF, SVT, VT
Define metabolic acidosis/alkalosis
Imbalance in production of acids or bases and their excretion by the kidneys
Common organisms causing pyelonephritis
E. coli most common
Klebsiella
Enterococcus
Pseudomonas
Causes of uraemia
Pre-renal:
Raised hepatic production of urea
Increased renal reabsorption
Iatrogenic
Renal:
Renal failure
Post-renal:
Urinary outflow obstruction
Define hypernatraemia
> 145mmol/L sodium
Clinical consequences at >155mmol/L
What findings are needed to confirm stage 1 or 2 CKD?
other than GFR
Albuminuria
Urine sediment abnormalities
Electrolyte and other abnormalities due to tubular disorders
Histological abnormalities
Structural abnormalities detected by imagine
History of kidney transplantation
Causes of end stage renal disease
Hypertension
Diabetes mellitus
Glomerulonephritis
How does diabetes affect the kidney?
Chronic high level of glucose passing through glomerulus causes scarring
Glomerulosclerosis
Management of UTI in pregnancy
7 days of antibiotics (even with asymptomatic bacteruria)
Urine for culture and sensitivities
First line: nitrofurantoin (avoid in 3rd T)
Second line: cefalexin or amoxicillin
