Kidney Flashcards
What is Chronic Kidney disease / Chronic renal failure?
(Subtle changes in kidney function) over period greater than 3 months
CHARACTERISTICS - reduction in GFR (less than 60 ml/min/1.73m2) - Proteinuria - Haematuria - proteinuria (more than 3 months)
RISK FACTORS 0 Hypertension 0 Diabetes 0 Autoimmune conidtions 0 long term analgesic use 0 etc.
MAIN CAUSES
0 Hypertension
Walls of artery supplying kidney thicken —————–> narrow lumen ———————-> Less blood & oxygen to supply the kidneys ————————-> Ischemia —————————–> Macrophages & foam cells secrete growth factors (e.g. TGF - B1 ) ————————-> cells regress back to immature state and secrete excess extracellular matrix (Mesangial cells to mesangioblasts ) ———————> Glomerulo - sclerosis ————————> diminished ability of kidney to filter blood.
0 Diabetes
Excess glucose —————-> glucose sticks to proteins (non -enzymatic glycation) ———————> effects BV e.g Efferent arteriole (carries blood away from glomerulus) of kidney (Hyaline arteriosclerosis - narrowing & more stiff) ———————–> Blood cannot leave glomerulus through efferent vessel (gets backed up)——————–> increase in pressure ———————–> Hyper filtration————————> High pressure state triggers mesnagial cells to secrete extracellular matrix ——————————> Glomerulo -sclerosis
OTHER CAUSES 0 Lupus , 0 Rheumatoid 0 arthritis 0 NSAIDS 0 Toxins e.g tobacco 0 Infection e.g HIV
Acute Kidney injury ?
Decrease in function within 3 months
Consquences of Chronic Kidney Disease?
- Azotemia
- Hyperkalemia —-> cardiac arrtmymias
- Hypercalemia ————> renal osteodystophy.
- Ethropoetin not produced by kidneys —————–> reduced RBC production——————-> anaemia
chronic kidney failure ———————–> reduced GFR —————–> urea builds up in blood (Azotemia - build up of nitrogenous waste e.g urea & creatinine in the blood - acts as poisons as they build up damaging tissue & organs )
Azotemia - symptoms e.g. Confusion - loss of appetite - decrease urine production - thirst cause by dry mouth -fatigue - pallor - swelling.
- Kidneys filter potassium , if GFR reduced K builds up in blood.
- Kidneys need to make Vitamin D ————–> reduced Vitamin D —————–> reduced absorption of CA ————————–> PTH released to compensate ———————-> Osteoclast activity increases , increased bone resorption
(renal osteodystrophy (weak and brittle bones) - bone disease where kidneys fail to maintain CA & Phospho levels
- Low CA levels ]- High PH levels
High PTH levels)
All these made worse by renin secreted by kidneys when GFR decreases (think there is low blood volume so increases pressure ) —–> Hypertension —————–> worsen kidney damage.
Symptoms of Chronic Kidney disease ?
Fatigue - linked to anemia & uremia (Azotemia )
0 Odema - reduced GFR leads to salt & water retention , made worse by possible hypoalbumineamia.
0 Nausea with / without vomiting - linked to Azotemia / build up of toxic waste products. May vomit
can report a metallic taste in their mouths.
0 Pruritis (itch) - toxic waste product accumulation in blood and under skin
0 restless leg syndrome - overwhelming urge to move legs - symptom of uraemia ( can be caused by other things tho - Dopmaine dysregulation)
0 Anorexia - toxic waste products
0 Weight loss
0 Impotence - erectile dysfunction.
(often these patients have narrowed BV - blood does reach penis so cannot get hard)
Arthralgia- JOINT PAIN - if has an autoimmune condition
Catergories of GFR deterioration ?
Stage 1 - eGFR - more than 90 with urinary or structural abnormality.
Treat BP and observe.
Stage 2 - 60 -90 - treat BP , risk factors and observe
Stage 3 A : 45 -60 B ; 30 -45 (overall 30-60) Treat BP and risk factors and observe
Stage 4- eGFR- 15 – 30
Renal replacement
planning
Stage 5 - eGFR < 15 Consider to initiate
dialysis
BP - ACE inhibitors (prils e.g ramipril, enalapril) , or Angiotensin II receptor blockers (sartans)
2ND LINE
Non 0 dihydropyridine Calcium Channel blocker
( class of calcium channel blocker that is more selective for cardiac muscle - more likely to cause cardiac depression & less potent vasodilation.
e.g.
0 Verampamil
0 Diliazem
(ADJUNCTIVE - additional antihypertensive therapy - if ACE or ARBs not sufficient e.g Beta-blockers , calcium channel blockers , spironolactone (potassium sparing diuretic) , Hydralazine (vasodilator)
PLUS - statin therpay (statins e.g sim/ atorvastatin)
IF DIABETIC
- Glycaemic control
Catergories of GFR deterioration ?
Stage 1 - eGFR - more than 90 with urinary or structural abnormality AND / OR persistent Haematuria, proteinuria, microalbuminuria. Treat BP and observe.
Stage 2 - 60 -90 - treat BP , risk factors and observe
Stage 3 A : 45 -60 B ; 30 -45 (overall 30-60) Treat BP and risk factors and observe
Stage 4- eGFR- 15 – 30
Renal replacement
planning
Stage 5 - eGFR < 15 Consider to initiate
dialysis (1st line)
2ND LINE
Kidney transplant
BP - ACE inhibitors (prils e.g ramipril, enalapril) , or Angiotensin II receptor blockers (sartans)
2ND LINE
Non 0 dihydropyridine Calcium Channel blocker
( class of calcium channel blocker that is more selective for cardiac muscle - more likely to cause cardiac depression & less potent vasodilation.
e.g.
0 Verampamil
0 Diliazem
(dihydropyridine - include amlodipine , felodipine etc)
(ADJUNCTIVE - additional antihypertensive therapy - if ACE or ARBs not sufficient e.g Beta-blockers , calcium channel blockers , spironolactone (potassium sparing diuretic) , Hydralazine (vasodilator)
PLUS - statin therpay (statins e.g sim/ atorvastatin)
IF DIABETIC
- Glycaemic control
WITH ANEMIA
- EPO stimulating agent
- iron supplements
WITH SECONDARY PARATHYROIDISM -
ADJUNCT dietary modification, phosphate binding drug
ADJUNCT - ergocalciferol - Vitamin D supplement.
WITH METABOLLIC ACIDOSIS
- oral sodium biphosphonate
What is Acute kidney injury ?
Decrease in kidney function within 3 months - usually over a few days - HIGH INDEX OF SUSPICISION (as often a silent disease until really bad)
CHARACTERISTICS
- Rise in serum creatinine
- Fall in urine output
Oliguria
RISK FACTORS
o Age - over 65 (particulary at risk)
o Myeloprolifertative disorder e.g. mutliple myeloma
o Previous AKI
o History of CKD , Heart failure , Diabetes , dementia etc - any neurological/ cognitive conditions that results in limited access to oral fluids
0 NSAIDS , aminoglycoside antibiotics , ACE /ARBs , Diuretic or other antihypertensie therapy started recently (e.g within last 7 days for ex) - risk of hypovolemia
0 Aciclovir ,methotrexate , triamterene . indavir , sulfonamides - risk of tubular obstruction by crystal formation.
0 Recent renal insult ( some kind of kidney injury ) e.g;
- recent surgery - kidney or cardiac/ recent vascular intervention.
- Hypovolemic episode
- Nephrotoxin use (NSAID, aminoglycoside)
SIGNS
Hypovolemia - Thirst, postural hypotension, dizziness.
- Oedema - peripheral (lower limbs hands and feet), peri-orbital (around eyes),
- Pulmonary edema
0 Crackles (on auscultation) - Tachypnoea - suggests fluid overload or acidosis (hyperventilation - body trying to get rid of CO2)
UNCOMMON
- Rash, fever, arthralgia If present suspect: 0 small vessel vasculitis, 0 granulomatosis with polyangiitis 0 microscopic polyangiitis), 0 interstitial nephritis.
- Haematuria
- enlarged prostate, palpable bladder, abdominal distension.
Pre - renal Causes of Acute Kidney injury ?
Different types of causes:
o Pre-renal (problem before the kidneys)
o intra-renal
o Post renal
NSAIDS & ACE inhibitors make it worse - NSAIDS block PG which dilate afferent vessels so loss of blood , ACE blocks —– which prevents constriction of efferent vessel- ALL OF THESE EFFECTS GFR.
Prerenal - decreased blood flow to kidneys e.g Hypotension, Hypovolemic states
o acute hemorrhage, o GI losses e.g diarrhea, o renal losses - diuretics or osmotic diuresis)
o Dermal losses
o Third space sequestration of fluid.
Can also be caused by Hypervolemic states ( high volume , but not circulating well )
o systolic heart failure - if this leads to AKI called Cardiorenal syndrome )
- Hypolbuminemia - if this leads to AKI called Hepatorenal syndrome
all have odeoma - so fluid is not circulating well.
Medications 0 NSAIDS 0 ACE 0 ARBs 0 Cyclosporine 0 Iodinated contrast. (cause damage to renal BV -------------------> ischemia ----------------------> pre-renal AKI)
IF GFR picks up after giving fluids is prerenal but if it does not - renal cause (acute tubular necrosis)
Causes of post-renal AKI?
POST RENAL - Obstruction of urine flow ----------------> urine build up -----------> pressure build-up CAUSES Prostatic cancer Benign Prostatic Hyperplasia (both compress urethra)
- Intrabdominal tumours that compress ureter.
- Kidney stones in ureter/urethra - if unilateral ureter (Kidney function often preserved vs bilateral ureter / blockage of urethra (only one of these)
may present with :
Lower urinary tract symptoms e.g
- Urinary urgency, hesitancy, , frequency.
CAN BE ASYMPTOMATIC - pressure build up , kidney wall hypertrophy or necrosis ?
arund 27 mins.
Causes of intrarenal AKI?
Intra renal - Damage to tubules , glomerulus, Interstitium (space btw tubules ) or vascular damage.
0 ATN - Acute tubular necrosis - damage to tubules due to ischemia (often from prerenal AKI) or nephrotoxin exposure (aminoglycoside antibiotics , methotrexate , Heavy metals, myoglobin (from damaged muscles - rhamdoylysis) , uric acid , radiocontrast dye, ethylene glycol.
0 Glomerular disease - damage to glomeruli
ex:
o IgA nephropathy (autoimmune condition)- IgA deposits builds up in kidney (Glomeruli) causing inflammation —————-> kidneys leak blood and protein——————–> scarring of nephrons ——————- can lead to end stage kidney/ Renal disease (ESDR)
(increased serum IgA level - signs Hematuria (common) +/- albuminuria)
0 Membranous nephropathy - immune system attack Glomeruli (filtering units in nephrons loacted in membrane of kidney— causes protein leakage - proteinuria)————————-> overtime progress to Nephrotic syndrome (acities , oedema)
similar idea : Membranousproliferative glomerulonephritis (MPGN)
o Glomerulonephritis - inflammation of the glomeruli
O MPGN - form of GN , antibodies deposit and build up in basement membrane damage it.——————–> proteinuria ————————> acities , oedema —————————> azotemia
(- Rapidly preogressive glomerulonephritis.
(small vessel vasculitis ,
good pastures - right properly)
Neurpathy I gA (usually benign - but in some can cause rapid loss of renal function) Infective endocarditis - write properly)
CAUSES
- Infection
- Cancer
- Autoimmune conditions e.g SLE , Sjogens, scleroderma, sacrodosis.
0 Nephritic syndrome - (signs and symptoms that occur with inflammation of kidney signs - Haematuria , (mild proturia - milder than nephtotic syndrome)
e.g causes - IgA neuropathy , Lupus nephritis (SLE )
0 Interstitial nephritis - inflammation of the interstitum (Type 1(immediate) or 4 (delayed - takes several days to develop)(sensitivity reaction) - usually in response to NSAIDS , Penicllins , Diuertics (thiazide) etc.
Renal artery stenosis
(symptoms - persistent hypertension - refractory to medication , oedema)
THINK ABOUT WHAT IS IN THE KIDEY —-> THEN WHAT COULD HAVE IF THEY WERE DAMAGE/ INJURED.
Tubules - ATN (necrosis ) , or can be come blocked by cancer , proteins (rhabdmyolysis)
BV - problems with veins , arteries , capillaries.
Glomeruli - Glomreulonephritis
Intersitiium - tubulo - intersitiual nephritis (intersititum becomes packed with immune cells ) - can cause AKI - TIN (can be caused by NSAIDS , antibiotics e.g penicllins , cephalsoproins ) , PPIS , multiple myeloma , sarcadosis,
TIN - treatment - reomve offending drug , steriods.
Stages of AKI ?
Stage 1 AKI: urine output
0 <0.5 mL/kg/h for at least 6 consecutive hours
0 rise in Creatinine 1.5 -1.9 x baseline (50 - 99% rise)
Stage 2 AKI: urine output
0 <0.5 mL/kg/h for at least 12 consecutive hours
CR
0 2- 2.9 x baseline (100 - 199)
Stage 3 AKI: urine output
0 <0.3 mL/kg/h for at least 24 consecutive hours or anuria for 12 hours
(ANURIA -kidneys do not produce urine - indicative of obstructive pathology or severe pre - kidney or intrinsic cause)
0 CR
more than 3 times baseline (200% x)
A higher stage of AKI is associated with a greater risk of death as well as an increased likelihood of needing renal replacement therapy (RRT).[
test for AKI?
Metabollic profile .eg. serum creatine, urea , LFTs (deranged in hepatorenal syndrome)
- rise in serum creatine (may take 24hrs for it to rise after kidney injury)
- BEWARE - Trimethoprim can caused increased creatine but no change in GFR.
- minor rises in serum Cr can represent a large loss in kidey function & increase in mortalilty.
Serum Potassium - increase
(if risen -ECG)
0 5.5 to 5.9 mmol/L indicates mild hyperkalaemia
0 6.0 to 6.4 mmol/L indicates moderate hyperkalaemia
0 ≥6.5 mmol/L indicates severe hyperkalaemia
- FBC - infection / sepsis - WBC rise.
anaemia. - Blood culture
- Urine culture
- Urinalysis
- Urine output monitoring - after AKI diagnoses.
- serum bicarbonate / venous blood gas (acidosis - caused by the body not get rid of enough acid)
- low bicarbonate
- CRP - elevated in vasculitis
- Fluid challange - if improved kidney function after suggest prerenal cause.
- CXR - pulmonary oedema, fluid, infection, cardiomegaly.
Differentiating btw CKD & AKI?
It is important to differentiate AKI from a progression of CKD at initial presentation.
Features that favour a diagnosis of CKD (although do not exclude AKI) include:
0 Hypocalcaemia
0 Hyperphosphataemia
High phosphate levels due reduced excretion causes increased calcitrol‐——) hypocalcemia and hyperparathyroidism
0 Anaemia - treated with regular subcateanous injections of erthopoietin.
0 Small kidneys on ultrasound (sometimes scarred) - suggestive of advanced CKD.
If the patient is acutely unwell or hypovolaemic, this points towards AKI
CKD is a risk factor for AKI.
Repeat blood testing along with reference to historical creatinine values is the key to confirming or ruling out AKI.
Treatment of AKI?
Hypovolemic
1st line - Fluid resuscitation
PLUS - medication - stop nephrotoxic drugs
- identify and treat underlying cause of AKI
o (obstructive - catheter)
o intrinsic (due to autoimmune causes) - immunomodulatory drugs , steriods , plasma exchange)
o removal of causative drugs medication review. - Vasoactive drug e.g Noradrenaline , vasopressin (if in shock e.g hypovolemic shock)
- Blood transfusion (if hypovolemia secondary to blood loss)
WITH METABOLLIC ACIDOSIS
0 Sodium Bicarbonate (risk of hypernaturemia)
severe - Kidney replacement
HYPERVOLEMIC
0 Sodium restriction
0 Loop diuretic - (with/out Pulomary oedema) - furesomide
Pulmonary oedema 1st line 0 Loop diuertic 0 sit patient upright 0 High oxygen - reservior mask 0 GTN
WITH HYPERKALEMIA
- insulin , glucose -push K intracelluarly.
- Nebulised salbutamol - to push K intracellularly
(Both used together in severe)
SEVERE - Calcium - protect heart against arrhythmias cause by HyperKAL
What are patients diagnosed with nephrotic syndrome at risk of ?
Deep vein thrombosis - loss of clotting factors and antithrombotic factors from the clotting cascade in the urine and hypovolaemia. There is also an increased susceptibility to infection due to loss of imunoglobulins in the urine.
same for membranous glomerulonephritis (small vessels in glomeruli become damage & thickened ———————-> proteins leak into urine (protein uria)———————–> can eventually lead to nephrotic syndrome.
