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77 Cards in this Set
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types of renal stones
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ca-oxalate (60% most common): radio opaque
cystine: cystinuria urate: not radioopaque mg-ammonium: associated with infections (klebsiella, proteus, ..) |
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haematuria - DDx
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renal tract (stones, tumors, infection, cyclophosphamide induced haemorraghic cystitis)
glomerulonephritis rhabdomyolysis malaria (blackwater fever) |
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suspected acute rejection of renal graft
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check ciclosporin levels - if normal need biopsy
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water deprivation test urinary osmolality
(result in DI, other cause) |
if not >750 then DI
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desmopressin test urinary osmolality
(result in central DI, nephrogenic DI) |
central DI: >50% increase after 2micromol desmopressin
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central pontine myolinolysis - how fast can you correct Na?
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1mmol/hour
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ACE-I and renal function - what's the catch?
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- non-progressive rise in creatinine 20-30% can be accepted
- guideline: check creatinine 1 week and 1 month - if deteriorates rapidly consider renal artery stenosis |
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diabetic nephropathy and pregnancy - change of deterioration?
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dending on creatinine there is a chance of worsening.
see study Katz et alhi |
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General points in measuring acute severe renal failure
(uraemic emergency, creatinine very high) |
1. sort out potassium if high
ECG -> if cardiotoxicity then Ca gluconade insulin+dextrose, neb salbutamol 2. sort out fluid status: urinary cathether CVP line start IV saline at 100ml per hour and titrate 3. further management: urgent USS liaise for renal replacement therapy |
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tubulointerstitial nephritis
causes |
70-90% drugs (penicillin, NSAIDs, etc)
15% infections (hantavirus - haemorrghic fever, pyelonephritis) 8% idiopathic TINU (with uveitis) systemic inflammatory disorders |
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tubulointestitial nephritis clinical features
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drug reaction 5 days - 5 months
fever, arthralgia, skin rashes, acute renal failure eosinophilia/eosinophiluria |
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chronic TIN causes
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analgetic abuse, DM, SSD
sloughed papillae can cause urinary obstruction. |
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tubulointestitial nephritis def
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inflammation affecting the interstitium around the tubules either acute or chronic
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consequences of TIN depending on location
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prox tubulus affected -> T2 renal tubulus acidosis
dist tubulus affected -> loss of concentrating function and salt wasting. general: loss of excretory function |
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TIN management & prognosis
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stop offending drug
steroid treatment not successful dialysis if severe renal function usually recovery but may have rresidual chronic impairment (degree of fibrosis) |
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analgetic nephropathy and flank pain and deterioration of renal function
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sloughed papillae
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renal artery stenosis causes
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fibromuscular disease 20-40%
artherosclerosis |
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artherosclerotic renal artery stenosis clinical features
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>60 years
30% in patient with other vascular manifestations patient with HTN, renal failure patient with flash pulm. oedema without cardiac disease clinical signs: abdominal bruit (or other vascular bruit incurring the possibility) |
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renal artery stenosis diagnosis
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ultrasound: difference in size >1.5cm, intrarenal vascular resistance to predict success of intervention
MRA/CTA |
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renal artery stenosis indications for revascularisation
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stenosis >75%
single functioning kidney recurrent flash pulmonary oedema intracable hypertension progressive renal failure patient requiring ACE-I for CCF |
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analgetic nephropathy and flank pain and deterioration of renal function
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sloughed papillae
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renal artery stenosis causes
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fibromuscular disease 20-40%
artherosclerosis |
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artherosclerotic renal artery stenosis clinical features
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>60 years
30% in patient with other vascular manifestations patient with HTN, renal failure patient with flash pulm. oedema without cardiac disease clinical signs: abdominal bruit (or other vascular bruit incurring the possibility) |
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renal artery stenosis diagnosis
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ultrasound: difference in size >1.5cm, intrarenal vascular resistance to predict success of intervention
MRA/CTA |
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renal artery stenosis indications for revascularisation
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stenosis >75%
single functioning kidney recurrent flash pulmonary oedema intracable hypertension progressive renal failure patient requiring ACE-I for CCF |
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when to investigate further in renal stones?
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young patient
recurrent stones |
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further investigations in renal stones
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serum Ca (hypercalcaemia -> investigate further if high)
uric acid (urate stones) HCO3-/urine pH (RTA) chemical analysis (cystine, urate stones) urine screening for cystinuria urinary calcium, oxalate and uric acid output urine culture renal imaging |
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prohpylaxis of renal stones
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adequate fluid intake (2-3L)
especially in cystine stones (5L) limit oxalate containing food (if oxalate stones) limit animal protein and salt (Ca stones) thiazide (ca stones) allopurinol (urate stones) penicillamine (cystine stones) |
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ADPKD complications
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cyst infection
renal calculi HTN progressive renal failure hepatic cysts 30% intracranial aneurysm 10% mitral valve prolapse 20% |
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ADPKD genetic basis
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PKD 1 on chromosome 16 85%
PKD 2 on chromosome 4 rest |
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ADPK presenting features
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acute loin pain, haematuria (bleeding, infection, stone in cyst)
general abdo discomfort and loin pain (cyst growing) complications of SAH complication of HTN complications of liver cysts chronic renal failure |
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medullary sponge disease clinical features
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intermittent renal colic with passage of small stones, haematuria
renal function is well maintained (unless obstructive uropathy ensues) |
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medullary sponge disease diagnosis
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diagnostic: excretion urography
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RCC def
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malignant tumor arising from proximal tubular epithelium
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RCC clinical features
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M>F 55yr (rarely before 40)
haematuria, loin pain, mass in flank rarely L sided varicocele with L sided tumour (invaded renal vein) 5% polycythaemia 30% HTN/anaemia 25% present with mets |
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RCC diagnosis
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USS/IVU may miss if <3cm
measure patency of renal vein and IVC MRI/CT for tumour staging urine cytology no value |
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RCC treatment
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nephrectomy (even if metastatic)
partial nephrectomy if solitary kidney IL2, beta-INF 20% remission |
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urothelial malignancy risk factors
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cigarrette smoking
carcinogens (chemical, rubber industry) chinese herbs (aristocholic acid) drugs (phenacetin, cyclophosphamide) schistosomiasis |
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TCC clinical features
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M>F >40yr
painless haematuria |
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TCC investigations
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urine cytology
cystoscopy (for lower urinary tract) USS/CT for upper urinary tract |
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TCC treatment
(bladder) |
superficial: transurethral resection, bladder instillarion for recurrences. 5-yr survival: 80-90%
invasive: <70yr radical cystectomy, >70 radical radiotherapy - 5% survival rate in metastatic disease. |
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benign prostate hyperplasia clinical features
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M >60
nocturia (first), frequency, hesitancy, reduced stream, post-void dribbling haematuria urinary retention/renal failure |
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BPH management
(mild sx, moderate sx, urinary obstruction) |
mild sx: watchful waiting
medium sx: medical Rx - tamsulosin, finasteride worsening renal failure: surgery urinary retention: either prostatectomy or perm. cath |
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Prostate Ca clinical features
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urinary tract obstruction
metastatic disease (bone) high PSA >16 in screening irregular hard gland on rectal exam |
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Prostate Ca investigations
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transrectal USS+biopsy
gleasson scoring based on histology USS (hydronephrosis) bone scan (metastasis) |
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Prostate Ca treatment
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confined to gland: radical prostatectomy
locally extensive: radio + androgen ablation metastases: orchidectomy/LHRH analogues |
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what is the "normal" renal function in patients in their 80s?
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GFR 50-60
cave: reduced muscle mass, hence creatinine falsly low. Use eGFR! |
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urinary incontinence
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urge incontinence (UTI, stone, stroke, dementia, PD)
stress incontinence (cough, sneeze) overflow incontinence funtional incontinence |
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incontinence management
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examine for local problems
urinalysis (glucose, culture for infection) Rx contributing factors: constipation, drug |
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urge incontinence
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bladder training, antimuscarinics (oxybutinine, tolterodine)
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stress incontinence
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pelvic floor exercises
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overflow incontinence
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treat obstruction
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functional
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improve facilities, regular voiding, absorbent padding
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causes of normal anion gap metabolic acidosis
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loss of bicarb in GI tract: diarrhoe
loss of bicarb renal: RTA Type 2, azetazolamide, ATN, hyperparathyroidism inability to excrete H+ renally: RTA Type 1 and 4 |
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normal anion gap
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10-18
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causes of Type 2 RTA
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Fanconis (glycosuria, aminoaciduria, phosphaturia, high urate excretion)
Wilson's hereditary fructose intolerance |
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osmolar gap
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osmolality = 2(Na+K)+glucose+urea
normal gap is <10 |
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what to do before epo therapy
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ensure iron storages are high
(ferritin >100) blood pressure is controlled |
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analgetic nephropathy
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= chronic TIN
60% have hypertension sloughed papillae can cause acute obstruction recurrent UTIs salt losing nephropathy |
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analgetic nephropathy findings
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IVU: clubbed calyces, ring signs, filling defects in urether
microscopy: papillary cells |
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management of malignant hypertension
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if signs of hypertensive encephalopathy or aortic dissection:
rapid BP reduction with IV nitroprusside/labetolol otherwise, oral antihypertensive aim for diastolic 100-120mmHg |
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management strategies for RCC
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nephrectomy even if mets
(exception - solitary kidney or bilateral tumor) IL2 or small molecule kinese inhibitors for mets radio or chemo no role! |
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causes of RTA type 1
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auto immune (e.g. SLE)
drugs (e.g. amphotericin) inherited idiopathic |
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management of RTA 1
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correct hypoK before acidosis!!!
bicarbonate 1-3mmol/kg per day to correct acidosis. |
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Familial mediterranean fever
clinical features |
autosomal recessive
Jews, Arab, Turk, Greece <18 years with first presentation fever and serositis that occurs in attacks (relapsing/remitting course): 95% abdominal attack: peritonitis (with all signs) 75% joint attack: arthritis, large joint 40% chest attack: pleuritis/pericarditis rare: scrotal attack, myalgia 25% fever alone |
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FMF complications
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AA amyloidosis leading to renal failure
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FMF diagnosis
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mainstay: clinical
CRP raised genetic test available |
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FMF management
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monitor renal function
treat symptomatically with NSAIDS colchicin 1-2mg can reduce attack frequency and amyloidosis. |
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Renal tubular acidosis type II associations
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Fanconi's, Wilson's, fructose intolerance, Lowe's, heavy metal poisoning.
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IgA nephritis diagnosis
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renal biopsy
NOT IgA levels! |
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Liddle's syndrome
clinical features |
autosomal dominant
presenting mostly with hypertension in childhood ENaC defect: uncontrolled Na reabsorption, hence K loss and metabolic alkalosis aldosterone low (response) |
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Liddle's treatment
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low sodium diet
amiloride |
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Renal tubular acidosis Type IV
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hyperkalaemic RTA
low aldosterone/failure to respond |
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RTA Type IV associations
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spironolactone, ACEI, ARB, trimethoprim, heparin, pentamin, NSAIDs
SLT, amyloidosis |
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How to manage early hyperparathyroidism in chronic renal disease? (Ca low-normal)
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if PTH > twice normal try alfacalcidiol
if not successful consider surgery. cinacalcet for patients who are not fit for surgery only (NICE) |
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How to manage anaemia in chronic renal disease?
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load iron storages
ferritin >100 start epo aim for Hb 10.5 - 12.5 |
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How to manage late hyperparathyroidism in chronic renal disease? (PTH high, Ca high)
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cinacalcet and low phosphate diet plus sevelamer
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