Nephrology Flashcards
Manifestations of high phosphate
Itch/pruitus
Osteodystrophy
Kidney stone disease name
Nephrolithiasis
Types of kidney stone composition
Calcium stones - either calcium oxalate, calcium phosphate.
Others:
Struvite (magnesium, ammonium, phosphate from bacterial infection)
Uric acid (low urine pH)
Cystine (genetic cause).
Risk factors for kidney calculi
Male Obese Dehydration Diet = high animal protein diet Deformity = horseshoe kidney Drugs = vitamin D supplements Diseases = hyperparathyroidism
3 common sites of renal stones
Pelvic-ureteric junction
Mid-ureter at cross over of iliac vessels
Vesicoureteric junction
Signs and symptoms fo renal calculi
Renal colic = sudden onset severe unilateral pain in the loin area and radiated to groin/labia area.
Pain can occur in spasms/intervals but usually constant.
Nausea, vomiting, haematuria.
Hx of dysuria, frequency or straining.
O/E - restless (peritonitis pts are still), pyrexi
Investigations for renal calculi
Non-contrast helical CT of KUB.
Urine dipstick = ++RBC
MSU for ms+c
FBC, CRP, U+Es, serum calcium, phosphate, urate
Pregnancy test in females
Management of renal calculi
1) Analgesia - IM diclofenac.
Anti-emetic - IM Metoclopramide.
2) Hydration - fluids will pass out stones <5mm.
3) Medical expulsion therapy for stones: CCB e.g. Nifedipine or alpha blocker e.g. tamsulosin.
4) ESWL - Extracorporeal shock wave lithotripsy.
5) Ureteroscopy and laser break down.
6) Surgical nephrolithotomy.
Types of polycystic kidney disease
Autosomal dominant (ADPKD) usually adult presentation. Autosomal recessive (ARPKD) much more rare and presents in childhood.
Genes in autosomal dominant polycystic kidney disease
PKD1 coding for protein polycystin 1 (85%) and PKD2 coding for polycystin 2.
Signs and symptoms of PKD
Can be asymptomatic until complication.
ADPKD = nocturia and polyuria ARPKD = childhood onset, abdo mass and renal failure, portal HTN and hepatic fibrosis..
History: Lumbar pain (esp females) Flank discomfort. Dysuria Haematuria LUTS e.g. urgency Symptoms of HTN e.g. headaches. FHx of PKD/ESRD. O/E: Palpable kidney/mass in flank area. HYPERTENSION
Investigations for PKD
KUB USS
Genetic testing.
CT abdo pelvis non-contrast.
Screen for complications:
- intracranial aneurysms with MRI
- ECG or echocardiogram.
Treatment of PKD
SCREEN FAMILY!
Ensure adequate water intake.
Treat symptoms e.g. HTN with ACE-i.
Renal replacement therapy - dialysis, transplant list.
Surgery on cysts
Genetic counselling.
Safety-net advise on SAH and cerebral aneurysms.
Glomerular filtration barrier components
Podocyte
Glomerular basement membrane
Fenestrated capillary endothelium
Flow of blood in nephron
Glomeruli –> proximal convoluted tubule –> descending loop of Henle –> ascending loop of Henle –> distal convoluted tubule –> collecting tubule –> collecting duct.
What makes up the renal corpuscle
Glomerulus and Bowman capsule
Name some functions of the kidney
Eliminate waste products Regulate acid-base balance Regulate blood pressure Regular electrolyte balance Produce erythropoietin Produce renin (juxtaglomerular apparatus) Activate vitamin D
Quick description of RAAS
- Low renal perfusion or increased sympathetic drive = kidneys produce RENIN.
- In liver angiotensinogen is converted to angiotensin I.
- Conversion of angiotensin I to angiotensin II via ACE mostly in lungs.
- Angiotensin II is vasoconstrictor.
- Aldosterone secretion of adrenal cortex under influence of angiotensin II.
- Aldosterone increases sodium and warmer reabsorption in kidneys.
Causes of end stage renal failure
Pyelonephritis
Polycystic kidney disease
Glomerulonephritis
Diabetes
Fanconi syndrome
- Proximal tubule dysfunction leading to acute tubular acidosis.
- Urine has high levels of:
Glucose, phosphate, uric acid, amino acid and high protein:creatinine ratio. - S+S: growth impairment, muscle weakness, Rickets, hypoglycaemia
- Ix: serum anion gap on ABG is normal.
- Rx: need to replace phosphate.
Hydronephrosis
Dilation of renal pelvis commonly due to urine obstruction.
Can be unilateral or bilateral.
If kidney function is affected from urine obstruction = obstructive nephropathy.
Common causes of hydronephrosis
Renal calculi (unilateral) BPH (bilateral) Prostate cancer Bladder cancer Iatrogenic e.g. gynae surgery
Presentation of hydronephrosis
Flank pain Dysuria LUTS Haematuria Fever
O/E:
Distended abdomen and palpable bladder
Ix for hydronephrosis and Mx
Lab:
Urea and creatinine
Urine dipstick
FBC
Imaging:
USS KUB
Non-contrast CT
Mx = treat cause. Analgesia, antibiotics. Ureteric stent, nephrostomy.
Why measure creatinine for kidney function
- Serum creatinine is usually constant.
- Creatinine is freely filtered by glomerulus and not reabsorbed so marker of GFR.
- Estimate GFR with serum creatinine level and a timed urine collection.
Definition for acute kidney injury 💦
Sudden onset renal dysfunction.
KDIGO definitions:
- Rise in creatinine >26micromol/L in 48hrs
- Rise in creatinine >1.5 times baseline creatinine within 7 days.
- Urine output <0.5ml/kg/hr for >6 consecutive hours.
Causes of acute renal failure
·PRE-RENAL = hypovolaemia, reduced cardiac output
e.g. burns, haemorrhage, cardiac failure, cariogenic shock, ACE inhibitors.
·RENAL = vascular glomerular, tubular and interstitial
e.g. thrombosis, scleroderma, glomerulonephritis, rhabdomyolysis, acute tubular necrosis due to SEPSIS, interstitial nephritis.
·POST-RENAL = obstruction
e.g. renal calculi, bladder cancer, BPH
·DRUGS (NSAID, contract, diuretics, ACE inhibitors, penicillins).
Acute tubular necrosis
- Decrease perfusion - sepsis, shock, contrast agents.
- VVVV common cause of intrinsic/renal AKI.
- Ix =Hyperkalaemia, hyperuraemia, high creatinine. Urinalysis = brown granular casts.
Name some nephrotoxic drugs 🤪
Iodinated contrast agents Diuretics ACE inhibitor and Angiotensin receptor blockers NSAIDS Gentamycin Acyclovir
Complications of AKI
Hyperkalaemia Metabolic acidosis Pulmonary oedema Uraemia CKD and ESKD
S+S of AKI
Decreased urine output
Nausea and vomiting
Dizziness, drowsiness, fatigue, altered mental state (uraemia).
Hx of risk factors or causes (DM, prescribed drugs, CHF, muscle cramps).
O/E:
tachycardia, hypotensive, pedal oedema.
AKI and not responsive to fluids cause…
Hepatorenal syndrome
Ix for suspected AKI
· Bloods: ABG or VGB, serum creatinine, U+E (esp potassium!!), LFT, FBC. Find cause e.g. ANCA, ANA antibodies, creatinine kinase (rhabdomylosis)
· Catheterise: urine dipstick, urine sample for microscopy (bence jones protein, cellular casts), urine osmolality, urine sodium.
· Other: ECG, CXR
· Imaging: KUB USS (within 24hrs)
Management of AKI
- Stop nephrotoxic drugs.
- A to E resuscitation including IV fluid bolus (500ml 0.9% normal saline STAT) and catheter.
- Investigate ABG + ECG + KUB USS + urine dipstick.
- Sodium bicarbonate for metabolic acidosis + good ventilatory support.
- If uraemia, severe met acidosis, severe hyperkalaemia = renal replacement therapy e.g. dialysis.
- If due to obstruction - stent.
- Consider need for ITU and vasopressors if not responding to fluid.
- RRT.
Management of hyperkalaemia and what level of K is worrying?
If potassium is >6.5mmol/L or >6mmol/L + ECG changes: ACT NOW 🆘⚠️🆘
·Nebulise salbutamol
·IV 10% calcium gluconate - repeat ECG. This protects the heart but does not treat high potassium.
·10units ACTRAPID + 50ml 50% glucose over 30mins - can do this twice before getting senior, specialist help.
Complications of polycystic kidney disease
Hypertension
Cyst infection
ESRF
Cardiac = aortic root dilation, mitral valve prolapse and other valvular diseases.
metformin and the kidneys
Won’t be exact cause of an AKI but will worsen the injury and increase acidosis.
Why metabolic acidosis in AKI?
Unable to excrete waste organic acids
Definition of chronic kidney disease
Chronic abnormal function or structure of the kidney which goes on for 3 months or more of:
- haematuria +/- proteinuria
- GFR <60ml/minute/1.73m2.
Common causes of CKD
Diabetes mellitus Glomerulonephritis Hypertension Polycystic kidney disease Nephrotic and nephritic syndromes; focal segmental glomerulosclerosis.
GFR and end-stage kidney disease
Stage 5 CKD = GFR <15ml/mine/1.73m2.
Who should be screened/routinely tested for CKD?
Diabetics HTN CHF or IHD SLE Recurrent UTI e.g. BPH
Presentation of CKD
Asymptomatic (apart from symptoms of causative disease), most picked up on routine checks.
Fatigue (anaemic)
Oedema (water and salt retention)
Nausea, pruritus and anorexia (uraemia)
Recurrent UTI
Investigating CKD
Serum creatinine Estimation of GFR using serum creatinine Albumin:creatinine ratio Urine dipstick Urine microalbumin KUB USS Look for cause - OGTT, BP, antibodies for glomerulonephritis cause. Prevent complications - FBC.
Management of CKD
1) Information, education and lifestyle advice: exercise, stop smoking, dietary advice (low salt diet).
2) Blood pressure control (target 140/90mmHg) e.g. ACE-inhibitor.
3) Optimum blood glucose control HbA1c <7%.
4) Prevent CVD in CKD patients with QRisk score and anti-platelet agent e.g. apixaban and statin.
5) Treat complications - ferrous sulphate for anaemia, diuretics for oedema, calcitriol or bisphosphonate for bone disease.
6) Stage 5 or uraemia = RRT.
Complications of CKD
Anaemia from reduced EPO action
Uraemia
Metabolic acidosis
Oedema
Low bone mineralisation (high phosphate, low vit D, secondary hyperparathyroidism)
Cardiovascular disease - left ventricular hypertrophy.
Hyperkalaemia
Monitoring of CKD patient
Annual creatinine for eGFR, urine dipstick.
Name some renal replacement therapies
Renal transplant
Peritoneal dialysis
Haemodialysis
What to do in the assessment of a patient for potential RRT?
Neurocognitive issues Psycho-social evaluation Understanding of process Interference with daily life Type of RRT patient has a preference for Is there a matched donor 👯♂️
Indications for dialysis in AKI
Uraemia Pulmonary oedema Severe hyperkalaemia Metabolic acidosis, unresponsive to sodium bicarbonate Severe renal failure.
Overview of haemodialysis
Requires AV fistula to bypass capillary network.
Blood passes over semi-permeable membrane in opposite direction to dialysis fluid.
Counter-current mechanism draws solutes out of blood into dialysis fluid along concentration gradient.
Constant infusion of heparin during procedure!
Need to come into hospital 3 times a week for around 4 hours.
Complications of haemodialysis
Infection
Hypotension
Disequilibration syndrome (tremor, fits, restless, coma)
Overview of peritoneal dialysis
Intermittent drainage and infusing.
Dialysate infused into peritoneal cavity and works with the semi-permeable peritoneum to filter solutes.
Ultrafiltration can be achieved by adding osmotic agents to the dialysate fluid e.g. glucose.
Need to do it twice a day but can be done at home, no admission.
Complications of peritoneal dialysis
Infection at catheter site
Peritoneal-dialysis related peritonitis
membrane function declines over time
Hernia
Possible sources for renal transplants and what needs to be matched
Deceased donor or living donor.
Match: ABO blood group, tissue HLA, antibody screening.
Contraindications for renal transplant
Cancer with metastasis
HIV with viral replication
Unstable CVD
Immunosuppression for renal transplant
Induction with basiliximab + IV methylprednisolone
Maintenance with prednisolone, calcineurin inhibitors e.g Tacrolimus and anti-metabolites e.g. Azathioprine.
Risks of renal transplant
Oppertunistic infections due to immunosuppression.
Surgical Cx e.g. thrombosis, infection, hernia.
Malignancy: post-transplant lymphoproliferative disorder, small increase in RCC.
Increased CVD risk
REJECTION - hyper-acute, accelerated, acute, chronic.
Young child with easy bruising, AKI symptoms and pale/anaemic. Hx of diarrhoea episode
· Haemolytic uraemia syndrome = microangiopathic haemolytic anaemia + thrombocytopenia (low platelets) + AKI.
· Shiga toxin-producing E.coli 0157:H7
· Ix = FBC, peripheral blood smear = schistocytes, serum creatinine, PT, stool sample for E.coli, U+E.
· Resuscitation with IV fluids, red cell transfusion, dialysis/RRT.
Accelerated HTN + AKI
Scleroderma renal crisis in patients with systemic sclerosis. Rapidly progressive glomerulonephritis.
Ix = kidney biopsy = onion skin thickening of arterioles, collapsed glomeruli.
Rx = ACE inhibitors, IV vasodilators.
Treatment of renal disease + small vessel vasculitis (?respiratory symptoms + renal symptoms)
High-dose glucocorticoids + cyclophosphamide/rituximab.
Diabetic nephropathy
Hyperfiltration, thickening of glomerular basement membrane and intercapillary glomerulosclerosis (Kimmelstiel-Wilson nodules).
Screen DM annually with
1) First-pass early morning urine specimen for estimation of the albumin:creatinine ratio
2) U+E for eGFR.
Common organism in pyelonephritis
E.coli
RFx for pyelonephritis
Hx of UTI DM Elderly Immunocompromised e.g. renal transplant, HIV. Sexual activity Anatomical deformity in kidneys Catheterisation
S+S of pyelonephritis
main 3:
Fevers
Flank pain
Costo-vertebral angle/renal tenderness
Vomiting
UTI symptoms e.g. cloudy urine, frequency, dysuria.
Ix and Mx for pyelonephritis
Ix = Urine dipstick, mid-stream urine sample microscopy, culture and sensitivity (incl gram stain), CRP, FBC, blood cultures, procalcitonin, KUB USS or CT.
Mx = adequate hydration, empiracal ABx until sensitivity known e.g. Ciprofloxacin.
What is glomerulonephritis?
Injury to glomerular capillaries and glomerular basement membrane cause proteinuria, haematuria and CKD.
Most are immune mediated injuries.
Most common glomerulonephritis
Focal segmental glomerulonsclerosis in nephrotic syndrome
Examples of nephrotic glomerulonephritis
Minimal change disease
Focal or segmental glomerulonephritis
Membranes nephropathy
Secondary causes e.g amyloidosis, SLE, HIV, diabetes.
Examples of nephritic syndromes
IgA nephropathy
Henoch-Schonlein Purpura
post-streptococcal glomerulonephritis
Anti-glomerular basement membrane disease
Pathophysiology of nephrotic syndrome
Proteinuria >3g/24hrs
Hypoalbuminaemia (<30g/L)
Peripheral oedema
Hyperlipidaemia
Non-proliferative
Pathophysiology of nephritic syndrome
Oligouria/AKI
Hypertension
Haematuria (red cells and casts)
Can have proteinuria but less than 3g/day
Inflammation
Proliferative
Investigating glomerulonephritis
Serum: FBC, U+E, albumin, creatinine (estimate GFR), LFT, CRP, autoantibodies, immunoglobulins, electrophoresis for complement, blood sugar.
Urine: dipstick, protein:creatinine ratio, microscopy for casts, mid stream urine MC+S.
BP
Renal USS
Renal biopsy.
Management of glomerulonephritis
Treat underlying cause!!
Fluid and salt restriction. Treat HTN (ACE inhibitor) Diuretics e.g. furosemide Corticosteroids Renal transplant
Minimal change disease
Not a massive cause of CKD Majority of patients are young children. Light microscopy = normal Electron microscopy = fusion of podocyte foot processes. Mx = prednisolone
Focal segmental glomerulosclerosis
Rx with high-dose prednisolone.
Control BP
Cause of CKD
Associated with HIV
IgA nephropathy
IgA antibodies deposit in mesangium.
S+S = haematuria, hypertension, <1g proteinuria, Hx of resp or GI infection.
Ix = biopsy shows IgA deposits in mesangium.
Rx = prednisolone, ACEi for BP.
Rash on extensor surface of legs, arthritis, high BP, low urine output
Henoch-Schonlein purpura.
Complications of Glomerulonephritis esp Nephrotic syndrome
Thromboembolism (high lipids)
UTI
Hypercholesterolaemia
Histology of renal cell cancer
Renal cell carcinoma, most are clear cell.
Proximal renal tubule epithelium in renal cortex.
Often seen as yellow because of high lipid content.
Mutation in Chr3 at VHL gene causes increase in IGF1 (angiogenesis and dysfunctional cell growth)
RFx for renal cell carcinoma
Male
Smoking
Obesity
Hypertension
Hereditary = Von Hippel-Lindau syndrome, polycystic kidney disease.
S+S of renal cell carcinoma
Asymptomatic
Abdominal mass Haematuria Loin pain Anorexia, malaise, weight loss. Left varicocele from left RCC compressing on venous drainage of left testis.
Paraneoplastic syndromes = HTN from renin, polycyathaemia from EPO, hypercalcaemia from PTHrP, Cushing’s from ACTH.
S+S of met to lung and bone.
Common locations to renal cell carcinoma to metastasis
LUNGS
Bone
Liver
Ix for renal cell carcinoma
Bloods: FBC - Polycythaemia from EPO, U+E, ESR, LFT.
Urine: cytology for red blood cells. Exclude UTI with mc+S.
Imaging: CT/MRI
Other: CXR for cannon-ball metastasis, skeletal survey for boney met.
∆ urine dipstick, KUB USS then CT (high enhancement of tumour).
Mx for renal cell carcinoma
Dependent on stage.
1) local tumour = laparoscopic partial or total nephrectomy.
2) If not suitable for invasive surgery consider radio-frequency or cryotherapy ablation.
3) Adjuvant monoclonal antibodies. Anti-VEGF biologics.
Complications of renal cell carcinoma
Compression of testicular vein = varicocele.
Paraneoplastic syndromes e.g. Cushing’s, Polycythaemia.
- Action of aldosterone?
2. Why do you get hypokalaemia and alkalosis in Conn’s?
- Distal convoluted tubule. Increase sodium reabsorption and potassium excretion.
- H+ is excreted along with potassium. If high potassium excretion will get loss of protons = alkalosis. Will get hypertension as high sodium retention leads water to follow.
What would an ABG and U+E show in Addisons?
Low aldosterone, less potassium and thus H+ excretion, less sodium reabsorption.
- Hyperkalaemia
- Acidosis
- Hypotension
Where do loop diuretics act?
Na+-K+-2Cl− symporter (NKCC2) in the thick ascending limb of the Loop of Henle.
Inhibit sodium, chloride and potassium reabsorption.
Where do thiazide diuretics act?
Inhibit of the sodium-chloride (Na/Cl) channel in the proximal segment of the distal convoluted tubule.
Have HTN resistant to Rx
Renal artery stenosis.
Kidneys are not well perfused from stenotic artery so activate RAAS despite rest of body adequately perfused.
Subarachnoid haemorrhage renal cause
Autosomal dominant polycystic kidney disease.
Can cause Berry aneurysms.
Someone has polycystic kidney disease, can you assess their risk of malignancy?
Bozniak staging
What do you need to do before dialysis and what are some complications?
Arteriovenous fistula.
Complications = infection, stenosis, thrombosis, Steal syndrome (ischaemia).
Indications for dialysis in AKI
Metabolic acidosis refractive to Rx (sodium bicarb) Hyperkalaemia Pulmonary oedema Uraemic pericarditis Severe uraemia
What is an amyloid deposit?
Histology specimen which binds to cotton wool dye, Congo red dye and shows green birefringence under polarised light.
Presentation of amyloidosis
Dependent on organ affected. Fatigue, weight loss, easy bruising, breathlessness, postural hypotension. Peripheral oedema. Massive proteinuria Hepatomegaly Heart failure, raised JVP Sensory glove + stocking polyneuropathy. Racoon eyes, peri-orbital purpura Carpel tunnel syndorme
Ix and Mx for amyloidosis
Biopsy of affected organ = stains red with Congo red dye, is green birefringence under polarised light.
Immunofixation electrophoresis.
Mx = symptomatic e.g. diuretics, beta-blockers.
May have role for chemotherapy or stem cell transplant.
What is amyloidosis a good ∆∆ for?
MGUS/myeloma.
Pathology of lymphoedema
Increased vascular permeability from inflammation.
Obstruction to lymph drainage.
Liver failure and nephrotic syndrome =
Hypoalbuminaemia and decreased oncotic pressure in plasma.
Acidotic with high chloride, low bicarbonate but normal anion gap…?
Renal tubular acidosis.
When do look at renal replacement therapy in CKD?
eGFR <15ml/min/1.73m2 (ESKD) or uraemia
Normal eGFR
eGFR >90 ml/minute/1.73 m2
Normal eGFR
eGFR >90 ml/minute/1.73 m2
Managing complications of CKD
- Anaemia
- CVD risk
- Osteoporosis
- Malnutrition
- Acidosis
- Oedema
- Hyperkalaemia
- Ferrous sulphate or if severe erythropoietin.
- Qrisk, statin, anti-platelet.
- Calciferol, bisphosphonate.
- Maintain healthy BMI, sodium salt restriction, exercise advise.
- Sodium bicarbonate.
- Loop diuretics
- Dialysis if over 7mmol/L
Uraemia clinical features and management
Symptoms:
Vomiting, nausea, fatigue, drowsiness, anorexia, pruritus, muscle cramps.
Altered mental state from uraemia encephalopathy
Signs: Uraemic frost on forehead and scalp Skin gets grey yellow tinge. Pallor Hypertension Elevated JVP Bruising Pericardial friction rub from pericarditis.
The causes of death in AKI
Volume overload e.g. flash pulmonary oedema
Metabolic acidosis
Hyperkalaemia
Chocolate or tea coloured urine in a catheter nag of an elderly patient who fell
Rhabdomyolysis.
Complications of nephrotic syndrome
Thromboembolic event e.g. DVT, MI
Infection e.g. cellulitis
AKI
Muddy brown cellular casts in urine
Acute tubular acidosis such as Fanconi’s syndrome
