Renal Flashcards
Patient with sepsis and AKI…what would ABG show?
And other common causes of this ABG
Septic patients often have raised serum lactate (due to hypoperfusion of peripheries). So metabolic acidosis with raised anion gap.
Raised anion gap is either increased production of decreased secretion of organic acids Eg
- –> lactic acid
- –> urate (renal failure)
- –> ketones
- –> drugs (salicylates, methanol)
Indicators for dialysis
A E I O U
–> Acidosis
–> Electrolyte disarray (^K, ^Ca, \/Na) esp when combined with AKI
–> Intoxicants
–>SLIME: Salicylic acid, Lithium, Isopropranol, Mg-containing
laxative, ethylene glycol)
–> Overload of fluid
–> Uraemia complications eg pericarditis, encephalopathy, GI bleeding
Chance of recurrence of nephrolithiasis in pt with Hx
More than 50% within 10yr
Patient 18-35yr old with haematuria two days after URTI
IgA Nephropathy
Renal referral
Treat BP and proteinuria with ACEi
Types of kidney cancer
renal cell carcinoma (ca of PCT)
transitional cell carcinoma (Ca of renal pelvis -prox part of ureters in kidney)
metastasis
How can you distinguish between enlarged spleen and kidney?
Kidneys are ballotable
Kidney usually resonant to perc (spleen dull)
Inspiration moves kidney vertically (spleen down and medially)
You can palpate above kidney (usually)
Spleen arises In left hypochondrium, below tip of 10th rib. Kidney is in lumbar region
Name and reason for J shaped scar?
Rutherford Morison scar for renal transplant
chronic kidney disease staging and how eGFR is measured
Creatinine may not be accurate due to difference in muscle so eGFR (includesCAGE creatinine, age, gender, ethnicity)
May be affected by:Pregnancy muscle mass and eating red meat
CKD 1 ➡️ Over 90ml/min, but kidney damage (abnormal U.E or proteinuria)
CKD 2 ➡️ 60-90 and kidney damage (abnormal U.E or proteinuria)
CKD 3a ➡️ 45-59
CKD 3b ➡️ 30-44
CKD 4 ➡️ 15-29
CKD 5 ➡️ less than 15… Dialysis or transplant may be needed
Causes of chronic kidney disease
Often no obvious causes… It is..HIDDEN. Biopsy if unsure though
70% are from diabetes, hypertension and atherosclerosis
Hypertension
Infection (eg ureteric reflux in childhood, chronic pyelonephritis,)
Diabetic Nephropathy
Drugs (eg analgesic Nephropathy)
Exotica (lupus, wegenermalaria)
Nephritis (glomerulonephritis, chronic pyelonephritis)
And adult PKD, Alports, myeloma
Examination findings of chronic kidney disease (signs not symp)
May have none ➡️ Pallor (chronic anaemia) ➡️ Lemon tinge to skin (uraemia) ➡️ Scratch marks (pruritus, uraemia) ➡️️ Hypertension ➡️ Pericardial rub (uncommon, from ureamia) ➡️️ Pleural effusion ➡️ Palpable kidney (PKD, hydronephrosis) ➡️ Bilat limb oedema ➡️ Rutherford Morison scar ➡️ AV fistula (or small umbilical scar from peritoneal dialysis)
Symptoms of chronic kidney disease
Often asymp
➡️ Fatigue (️anaemia, psychosocial, accumulation of waste products)
➡️ Breathless (️anaemia, HF(hypertension etc), fluid overload)
➡️ Restless leg syndrome (common, uraemia -can treat with dop agonists)
➡️ pruritis (phosphate retention¿)
➡️ Bone pain (low vit D due to lack of 1-alpha hydroxylation, phosphate retention, reduced calcium absorption….all lead to increased PTH)
➡️ Anorexia vomiting and metallic taste (uraemia)
➡️ Leg swelling / weight gain (fluid retention)
➡️ Secondary gout from urate retention
What options are available if need dialysis but can’t wait 6 weeks for AV fistula to form an arterialised vein
Dual lumen tunnelled cuffed catheter (usually placed in internal jugular vein)
Problem: high recirculation rate
What vessels are AV fistulaes cmmononly made with
Usually radiocephalic, or ulnarbasilic
Brachiocephalic also possible
What is the physiology behind oedema in liver failure and kidney failure
Both result in hypoalbuminaemia. This reduces oncotic pressure so fluid moves into intracellular space
Bone disease in chronic renal disease…three main bullet points
➡️ renal damage causes loss of 1-alpha hydroxylase…so low Vit D
➡️ reduced Ca absorption in gut (due to vit d def)
➡️ renal damage causing phosphate retention
………….so hypocalc and hyperphos causes secondary hyperparathyroidism
…. This results in increased reabsorption from bone and increased proximal renal reabsorption
- increased osteoclastic activity, cyst formation, bone marrow fibrosis
Look out for bone pain, brachydactyly,
“Rugger Jersey spine” lateral spine X-ray has lines of sclerotic end plates and Lucent central area
Insulin requirements in diabetic patients as chronic renal failure progresses
Insulin requirements decrease because insulin is catabolised and to some extent excreted by kidney…
Complications of chronic renal disease (increased decreased) and features (big bean)
Increased,,,….
…urate retention so gout
…phosphate retention so hyperparathyroidism and pruritis
…increased catecholamine so anorexia neuropathy
Reduced…….
…reduced EPO so anaemia
…reduced activated vit D so osteomalacia
…reduced renin system so hypertension
Cardiovascular… Overlapping risk factors, but also Hyper phosphate increases risk
Breathlessness Itching Gout Bone pain (osteo dystrophy) Energy levels low Ankle swelling /anaemia Neuropathy
Spot diagnosis of continuous ambulatory peritoneal dialysis and what sort of problems do these patients have?
Indicated in end stage renal failure.
During CAPD, dialysate is put into your abdomen four times a day for 30mins through a Tencknoff catheter
Peritoneum acts as a partially permeable membrane and filters out U+E, K, phos, along conc gradient and water along osmotic gradient.
Issues?
Psycho social, permanent catheter. Time, can do at home though
Infection, malaise
Take EPO, vit, iron,BP, medications, insulin if diabetic
Nephrotic syndrome features and management
➡️ Proteinuria over 3g per 24h (partly cause damage allows leak
➡️ Hypoalbuminaemia under 30g/dL
➡️ Oedema (loss of oncotic pressure allows salt and water into extrac)
➡️ Hypercholesterolaemia as liver makes more chol (linked to compensatory increased albumin synth)
Reduce dietary sodium and have normal protein
Thiazide
ACEi (reduce proteinuria by decreasing glom filtration rate)
60mg pred if minimal change disease
Pt treated for impetigo with Fluclox. One week later has very dark urine, likely cause?
Post streptococcal glomerulonephritis…usually 7-14 days after.
Unclear mechanism, but believed to be a type III hypersensitivity reaction, immune complexes become lodged in the GMB and compliment activation results in destruction of this membrane.
Features: headaches, malaise, haematuria, nephritic syndrome, low complement (unlike IgA)
Smokey brown haematuria with red cast cells
Hypertension
Oligouria
Proteinuria
Minimal change disease causes and investigation
70-80% unknown!
Can be drugs like NSAIDs, rifampacin,
Hodgkins, thymoma, glandular fever
T cell mediated damage to GBM, resulting in polyanion loss
…this loss of electrostatic charge allow leaking of albumin
Normal electron microscopy, or fusion of foot processes of podocytes
Response to high dose prednisolone helps confirm
Causes of nephrotic syndrome
Primary glomerular disease: ...MCD (commonest in children) ...membranous Nephropathy (commonest in adults, esp if malig, autoimmune, infection(HBV, HCV, HIV,) drugs (gold, penicillamine, NSAIDs) ...congenital (auto recessive) Secondary ...diabetic Nephropathy ...amyloidosis ...SLE ...HSP
Investigation for CKD to assess severity
Urine microscopy - look for infection and for “casts”-may suggest glomerulonephritis, bence Jones - myeloma
Fbc - normocytic normochromic anaemia
Urea creatinine - poor correlation with GFR though (so better to do eGFR)
Creatinine clearance - 24hr urine collection with blood sample
Serum urate and phos
Low calcium and high alp suggestions osteodystrophy
Blood tests for Hep b, antinuclear factor, etc
Axr may show calcification stones or renal tuberculosis
USS to exclude obstruction and pckd
IVU - looking for renal artery stenosis, dilated pelvic calyces and cortical scarring (chronic pyelo), loss of papillae (analgesic nephropathy)
IVU suggesting chronic pyelonephritis
dilated pelvic calyces and cortical scarring
