Renal Flashcards
What are the causes and risk factors of chronic kidney disease?
- Diabetes, hypertension, older age, glomerulonephritis, PCKD
- Medications-> NSAIDs, PPIs, lithium
How does chronic kidney disease usually present?
Asymptomatic, itching, loss of appetite, nausea, oedema, muscle cramp, peripheral neuropathy, pallor, hypertension
What are the investigations for chronic kidney disease?
- eGFR via U+Es-> 2 tests 3 months apart
- Proteinuria-> urine albumin:creatinine (>3mg/mmol is significant)
- Haematuria-> dipstick, 1+ is significant (warrants malignancy investigation)
- Renal US-> obstruction etc
What are the stages of CKD and what are they based on?
Look at eGFR + albumin:creatinine ratio
- eGFR-> >90 (1), 60-89 (2), 45-59 (3a), 30-44 (3b), 15-29 (4), <15 (5)
- Albumin-> <3mg/mmol (1), 3-20 (2), >30 (3)
When is CKD diagnosed?
When eGFR <60 or proteinuria
What are the complications of CKD?
Anaemia, renal bone disease, CVD, peripheral neuropathy, dialysis problems
How is CKD managed?
- Reduce CVD + complication risks-> atorvastatin 20mg + weight
- Refer to specialise when meet criteria
- Treat glomerulonephritis
- Optimise diabetes + HTN treatment
- Sodium bicarb-> for metabolic acidosis
- Iron + erythropoietin-> for anaemia
- Vitamin D
What are the criteria for referral to a specialist in CKD?
- eGFR <30
- ACR >70
- eGFR decreases by 15 or 25% or 15ml/min in 1 year
- Uncontrolled HTN after 4+ medications
How is hypertension managed in CKD?
- ACE-i’s 1st line
- Aim for BP <140/90 or <130/80 if ACR >70mg/mmol
- Monitor serum K+-> hyperkalaemia risk
Why does anaemia occur in CKD?
Erythropoetin deficiency in CKD-> RBC production lower
How is anaemia in CKD managed?
- Exogenous EPO
- Transfusions-> can get allosensitisation
- IV/oral iron
What is renal bone disease and why does it occur?
- Osteomalacia, osteoporosis and osteosclerosis
- High serum phosphate due to reduced excretion
- Low vitamin D as not metabolised to active form-> calcium absorption + bone turnover not regulated
- Low calcium + high phosphate causes pituitary to excrete more PTH-> more osteoclast activity-> absorb calcium from bone-> secondary hyperparathyroidism
What are the X-ray changes seen in renal bone disease?
Vertebral sclerosis, osteomalacia in centre of vertebrae (rugger jersey sign)
What causes osteomalacia in renal bone disease?
Increased turnover without adequate calcium
What causes osteosclerosis in renal bone disease?
Osteoblasts increase activity to match osteoclasts but low calcium means tissues not mineralised properly
What causes osteoporosis in renal bone disease?
-Can be a co-morbidity eg due to age or steroids
How is renal bone disease managed?
Give active vitamin D + bisphosphonates
What is the function of the kidney?
- Filter + excrete waste products from the blood-> urine
- Water and electrolyte balance
What is the anatomical position of the kidneys?
- Retroperitoneal
- Extend from T12 to L3
- Adrenal glands superior to the kidney within renal fascia
What is the internal anatomy of the kidney (ie the different layers)?
- Outer cortex + inner medulla
- Renal pyramids-> cortex extending into medulla + dividing it into triangles
- Renal papilla-> apex of renal pyramid
- Minor calyx-> collects urine from oyramids
- Major calyx-> minor calices converge to form one + where urine passes through
- Renal pelvis-> where urine drains to ureter
- Renal hilum-> where renal vessels + ureter enter/exit
What is the arterial blood supply of the kidneys?
- Renal arteries-> directly from abdominal aorta
- Renal artery-> anterior + posterior division-> 5 segmental ateries from these
What is the venous drainage of the kidneys?
- Left + right renal veins
- Left renal vein-> longer as IVC sits more to right
What are the different parts of the nephron?
- Glomerulus ie Bowman’s capsule
- Proximal convoluted tubule
- Loop of Henle
- Distal convoluted tubule
- Collecting duct
How does the glomerulus of the kidney work?
- Not permeable to plasma proteins
- Permeable to sodium, potassium, amino acids, creatinine etc
What are the definitions/criteria of acute kidney injury?
- Acute drop in function measured by serum creatinine
- Rise in creatining of >25micromol/L in 48 hours
- Rise in creatinine of >50% in 7 days
- UO of <0.5ml/kg/hour for >6 hours
What are the risk factors for acute kidney injury?
Acute illness, infection, operations, older, cognitive impairment, CKD, HF, DM, liver disease, NSAIDs, ACE-i’s, contrast medium for CTs
What are the three types/causes of AKI?
Pre-renal, renal and post-renal
What are the causes of pre-renal AKI?
Inadequate blood supply-> dehydration, hypotension, heart failure
What are the causes of renal AKI?
Intrinsic kidney disease, glomerulonephritis, interstitial nephritis, acute tubular necrosis
What are the causes of post-renal AKI?
Obstruction + back pressure-> stones, cancer, strictures, BPH, prostate cancer
What is the most common type/cause of AKI?
Pre-renal
What are the investigations for AKI?
- U+Es-> creatinine rise, electrolyte imbalance etc
- Urinalysis-> leucocytes + nitrites (infection) or protein + blood (acute nephritis, infection) or glucose (diabetes)
- Ultrasound-> obstruction
What is the management of AKI?
- Prevention-> IV fluids + avoid nephrotoxic meds
- Treatment-> fluids, stop meds, relieve obstruction
- If severe-> renal input + dialysis
What are the potential complications of AKI?
Hyperkalaemia, fluid overload, HF, pulmonary oedema, metabolic acidosis, uraemia leading to encephalopathy or pericarditis
What is dialysis?
Artificial filtration of the kidneys in end stage disease-> remove fluid, solutes and waste
What are the indications for acute dialysis?
AEIOU
- Acidosis
- Electrolytes (eg hyperkalaemia)
- Intoxication
- Oedema
- Uraemia (symptoms- seizure, reduced consciousness)
Indications for long-term dialysis?
CKD stage 5, acute indications long term (AEIOU)
What is peritoneal dialysis?
- Add dialysis solution + dextrose to peritoneal cavity-> ultrafiltration from blood across peritoneal membrane to solution-> replace + take away waste
- Can be continuous ambulatory-> solution in at all times ie 2 fluid 4x daily
- Can be automated-> overnight for 8-10 hours
What are the potential complications of peritoneal dialysis?
Spontaneous bacterial peritonitis, peritoneal sclerosis (scarring), ultrafiltration failure, weight gain, psychosocial implications
What is haemodialysis?
- Blood filtered
- 4 hours ish 3 times a week
- Some-> catheter in subclavian/jugular vein + sits in SVC or RA long term
- Some-> AV fistula
What is an AV fistula in the context of haemodialysis
- Surgical operation-> connection by bypass capillaries + flow under high pressure from artery to vein
- Usually radio-cephalic, brachio-cephalic or brachio-basilic
What clinical signs might someone with an AV fistula have?
Machinery murmur + thrills
What are the complications of an AV fistula?
- Aneurysm, infection, thrombosis, stenosis
- STEAL syndrome-> inadequate blood flow distally (‘steals’ from limb) so flows into venous system + cause distal ischaemia
- Heart failure as flow quick from arterial to venous-> rapid return to heart-> increase preload + hypertrophy
What are the benefits of renal transplant?
In end stage renal failure adds 10 years compared to with just dialysis
How are donors matched in renal transplant?
- Based on human leucocyte antigen (HLA) types A, B and C
- Don’t have to fully match-> can get desensitisation treatment
What scar might be present in someone who’s had a renal transplant?
- Hockey stick incisional scar
- Can palpate kidney in iliac fossa
What do patients require after a renal transplant?
Lifelong immunosuppression regime to reduce rejection risk-> tacrolimus + mycophenolate + prednisolone
What are the potential complications of renal transplant?
- Rejection-> hyperacute, acute, chronic
- Failure
- Electrolyte imbalances
- Related to immunosuppressants-> T2DM, HIS, infections, non-Hodgkin lymphoma, skin cancers
What is glomerulonephritis?
Non-specific inflammation of the kidneys-> umbrella term
What is nephritic syndrome and what are its features?
- A group of symptoms not a diagnosis
- Haematuria-> micro or macroscopic
- Oliguria-> reduced UO
- Proteinuria-> <3g in 24 hours
- Fluid retention
What is nephrotic syndrome and what are its features?
- Group of symptoms without a specific cause
- Peripheral oedema
- Proteinuria-> >3g in 24 hours
- Serum albumin <25g/L
- Hypercholesterolaemia
What is the typical presentation of nephrotic syndrome?
Oedema and frothy urine (due to proteinuria)
What are the complications of nephrotic syndrome?
Pre-disposition to thrombosis, hypertension and hypercholesterolaemia
What type of nephrotic syndrome is most common in kids?
Minimal change disease
How is minimal change disease managed?
Steroids-> usually idiopathic
How is the most common type of nephrotic syndrome in adults?
Focal segmental glomerulosclerosis?
What are the different types of glomerulonephritis?
- Nephrotic and nephritic syndromes fit into this
- Minimal change disease, focal segmental glomerulosclerosis, membranous glomerulosclerosis, IgA nephropathy, post-strep glomerulonephritis, Goodpasture syndrome
What is the most common primary glomerulonephritis?
IgA nephropathy
What are the features of IgA nephropathy?
- Peaks in 20’s
- IgA deposits + glomerular mesangial proliferation on histology
What are the features of membranous glomerulonephropathy?
- Presents in 20’s and 6’s
- 70% idiopathic
- Some due to NSAIDs and cancers
- IgG and complement deposits in basement membrane
What are the features of post-streptococcal glomerulonephritis?
- Presents in under 30’s
- 1-3 weeks after strep infection-> tonsillitis or impetigo
- Nephritic syndrome
- Usually make full recovery
What are the features of Goodpasture syndrome?
- Anti-GBM antibodies attack glomerulus + pulmonary basement membranes
- Glomeruponephritis + pulmonary haemorrhage
- AKI + haemoptysis
- Can cause rapidly progressive glomerulonephritis
What are the features of rapidly progressive glomerulonephritis?
- Acute illness
- Often secondary to Goospasture’s
- Histology-> crescentic
- Responds well to treatment
What is interstitial nephritis?
- Inflammation of interstitium of kidney-> between cells + tubules
- Different to glomerulonephritis
- Acute or chronic
What is glomerulosclerosis?
Damage and scarring of glomerulus tissue due to other pathology
What can cause glomerulosclerosis?
- Glomerulonephritis
- Obstructive uropathy
- Focal segmental glomerulosclerosis
How are most types of glomerulosclerosis treated?
- Steroids-> for immunosuppression
- ACE-is or ARBs-> BP control + block RAAS
What is the pathology behind diabetic nephropathy?
Glomerulosclerosis-> chronic passing of high levels of glucose through glomerulus causes scarring
What is the main feature of diabetic nephropathy?
Proteinuria-> damage causes leakage into urine
How is diabetic nephropathy screened for?
- Albumin:creatinine ratio
- U+Es
How is diabetic nephropathy managed?
- Optimising BMs and blood pressure
- ACE-i’s-> start when nephropathy regardless of BP level
What is acute interstitial nephritis?
- Inflammation of space between kidney cells + tubules (interstitium)
- AKI and HTN due to acute inflammation
What is the presentation of acute interstitial nephritis?
- Rash
- Fever
- Eosinophilia
- AKI
- HTN
- Can be reaction to NSAIDS or antibiotics or due to infection
How is acute interstitial nephritis managed?
- Treat the underlying cause
- Steroids
What is chronic tubulointerstitial nephritis?
- Inflammation of space between cells + tubules (interstitium)
- CKD due to inflammation
What causes chronic tubulointerstitial nephritis?
AI, infection, iatrogenic
How is chronic tubulointerstitial nephritis managed?
- treat the underlying cause
- steroids
What is acute tubular necrosis?
- Damage + necrosis of epithelial cells in tubules
- Reversible as epithelium regenerates
- Common cause of AKI
What can cause acute tubular necrosis?
- Hypoperfusion-> shock, sepsis, dehydration
- Toxins-> radiology contrast dye, gentamycin, NSAIDs
How is acute tubular necrosis investigated?
Urinalysis-> muddy brown casts (pathognomonic) + maybe renal tubular epithelial cells
How is acute tubular necrosis managed?
Supportive-> IV fluids, stop meds, complication management
What is renal tubular acidosis?
- Metabolic acid due to pathology in tubules
- Tubules usually balance H+ and bicarb ions between blood + urine to maintain pH-> pathology causes issues
What is type 1 renal tubular acidosis?
Distal tubule pathology-> unable to excrete H+
What causes type 1 renal tubular acidosis?
Genetic, SLE, Sjogren’s, PBC, hyperthyroidism, sickle cell, Marfan’s
How does type 1 renal tubular acidosis present?
FTT, hyperventilation (to compensate for acidosis), CKD, osteomalacia
What blood and urine results may be apparent in type 1 renal tubular acidosis?
- Hypokalaemia + acidosis
- Acidic urine (pH 6 or more)
What is the treatment for type 1 renal tubular acidosis?
Oral bicarbonate-> correct electrolyte imbalances
What is type 2 renal tubular acidosis?
Proximal tubule pathology-> unable to resorb bicarbonate so excess in urine
What is the main cause of type 2 renal tubular acidosis?
Fanconi syndrome
What is the management of type 2 renal tubular acidosis?
- Bloods-> hypokalaemia + acidosis
- Urine-> acidic urine (pH 6 or more)
- Give oral bicarbonate-> correct electrolyte imbalances
What is type 3 renal tubular acidosis?
A mixture of type 1 and 2 renal tubular acidosis-> very rare
What is type 4 renal tubular acidosis and what can cause it?
Renal tubular acidosis due to reduced aldosterone-> adrenal insufficiency, ACE-is, spironolactone, SLE, diabetes, HIV
Which is the most common type of renal tubular acidosis?
Type 4
What investigations are done in renal tubular acidosis?
- Bloods-> hyperkalaemia, high chloride, metabolic acidosis
- Urine-> low pH
How is type 4 renal tubular acidosis managed?
- Fludrocortisone
- Sodium bicarb
- Hyperkalaemia treatment if present
What is haemolytic uraemic syndrome?
Medical emergency in which many thrombi occur throughout the body-> often triggered by shiga toxin (E.coli + Shigella)
What is the pathophysiology of haemolytic uraemic syndrome?
- Triggered by shiga toxin-> from E.coli 0157 or shigella
- Blood clots consume platelets-> thrombocytopaenia
- Clots chop up RBCs as pass by-> haemolysis + anaemia
- Blood flow through kidneys affected by clots + damaged RBCs-> AKI
What infections often trigger haemolytic uraemic syndrome?
- Shiga toxin-> from E.coli 0157 or Shigella
- Higher risk if antibiotics or anti-motility medications used
How does haemolytic uraemic syndrome present?
- E.coli infection-> gastroenteritis + bloody diarrhoea
- 5 days after-> reduced urine output, haematuria or dark urine, abdominal pain, lethargy, confusion, hypertension, bruising
- ‘Triad’-> haemolytic anaemia + AKI + thrombocytopaenia
What is the ‘triad’ of pathologies that occur in haemolytic uraemic syndrome?
Haemolytic anaemia + AKI + thrombocytopaenia
How is haemolytic uraemic syndrome managed?
- Self limiting illness
- Supportive-> anti-HTNs, transfusions, dialysis
What is rhabomyolysis?
Break down of skeletal muscle + release of products into blood due to extreme underuse, overuse or trauma
What is the pathophysiology of rhabdomyolysis?
- Extreme under or overuse or trauma-> skeletal muscle breaks down + releases products
- Myocytes apoptose-> release myoglobin, potassium, phosphate and CK into blood
- Cause hyperkalaemia-> arrhythmias
- Cause myoglobulinaemia-> toxic to kidneys in high concentrations-> AKI + accumulation
What causes rhabdomyolysis?
- Anything that can damage cells
- Prolonged immobility-> frailty + falls
- Rigorous exercise
- Crush injuries
- Seizures
- Statins
What are signs and symptoms of rhabdomyolysis?
Muscle aches, oedema, fatigue, confusion, red-brown urine
What are the investigations for rhabdomyolysis?
- U+Es-> AKI + hyperkalaemia
- ECG-> for hyperkalaemia
- Urine dip-> red-brown with +ve for blood (myloglobinurea)
- Blood CK-> very high, rise till 12 hours, stay up for 1-3 days, then gradually fall
How is rhabdomyolysis managed?
- IV fluids-> rehydrate + encourage breakdown product filtration
- IV sodium bicarb-> make urine more alkaline + reduce myoglobin toxicity
- IV mannitol-> after correcting hypovolaemia to increase eGFR + reduce oedema
- Treat complications
What are the causes of hyperkalaemia?
- AKI, CKD, rhabdomyolysis, adrenal insufficiency, tumour lysis syndrome
- Meds-> NSAIDs, ACEis, ARBs, aldosterone antagonists (spironolactone etc)
What investigations should be done in hyperkalaemia?
- U+Es-> K+, creatinine, urea, eGFR
- ECG-> need when K+ >6mmol/L + may see tall peaked T-waves, flattened/absent P waves, broad QRS
What ECG findings may be present in hyperkalaemia?
Tall peaked T-waves, flattened/absent P waves, broad QRS
How is hyperkalaemia managed?
- Local policy, close ECG monitoring + renal input
- Need urgent treatment if >6mmol/L K+
- Calcium gluconate-> stabilise cardiac muscle cells + reduce arrhythmia risk
- Insulin + dextrose-> drive carbs into cells + take K+ in to reduce blood levels
- Nebulised salbutamol
- IV fluids-> increase UO + encourage K+ loss
- May use oral calcium resonium, sodium bicarbonate, dialysis
What is polycystic kidney disease?
Genetic condition in which kidneys develop cysts leading to significant impairment and sometimes extra-renal problems
What are the different types of polycystic kidney disease?
- PKD-1-> autosomal dominant (chromosome 16)
- PKD-2-> autosomal dominant (chromosome 4)
- Autosomal recessive polycystic kidney disease (ARPKD)-> chromosome 16
What extra-renal manifestations can occur in autosomal dominant polycystic kidney disease?
- Cerebral aneurysms
- Cysts-> hepatic, splenic, pancreatic, ovarian, prostatic
- Mitral regurgitation
- Colonic diverticula
- Aortic root dilatation
What are the complications of autosomal dominant polycystic kidney disease?
Chronic loin pain, HTN, CVD, gross haematuria (eg cyst rupture), renal stones, end stage renal failure
What is the presentation of autosomal recessive polycystic kidney disease?
- Oligohydramnios-> as foetus doesn’t produce enough urine
- Underdeveloped lungs + respiratory failure after birth
- Dysmorphic features-> low set ears, flat nasal bridge
- End stage renal failure before adulthood
How is autosomal recessive polycystic kidney disease managed?
-May need dialysis in first few days of life
How is polycystic kidney disease diagnosed?
- Ultrasound
- Genetics
How is polycystic kidney disease managed (in general)?
- Tolvaptan-> vasopressor receptor antagonist, can slow cyst developement
- Complications support-> anti-HTNs, analgesia (colic), antibodies/drainage of infected cysts, dialysis, transplant
- Avoid contact sport-> cyst rupture
- Avoid anti-inflammatories + anti-coagulants
- Regular US + bloods + BP monitoring
- Regular MR angiograms-> cranial aneurysms
- Genetic counselling
