Diabetic nephropathy. Diabetic nephropathy- definition Chronic microangiopathy type complication of DM characterized by: 1. proteinuria 2. hypertension.

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Presentation transcript:

Diabetic nephropathy

Diabetic nephropathy- definition Chronic microangiopathy type complication of DM characterized by: 1. proteinuria 2. hypertension 3. progressive loss of GFR leading to ESRD

Microalbuminuria 1. albumin excretion in urine 30 – 300 mg/d or 20 – 200 ug/min 2. If temporary, but >80 mg/d it means in 95% progression to continuous microalbuminuria 3. If continuous - it means threatening nephropathy. Not treated increases 20 – 40% a year. After 5 years becomes macroalbuminuria = evident diabetic nephropathy

Macroalbuminuria 1. Albumin excretion in urine >300 mg/d 2. It may lead to development of nephrotic syndrome (proteinuria, hypoalbuminaemia, hyperlipidaemia, edema) 3. ESRD appears usually after 5 years

Time course of DN according to type of DM (Mogensen scale) IDDM NIDDM IDDM NIDDM I stadium (0-2 yrs) hyperfiltration (100%) (unnoticeable) II stadium (2-5yrs) silent DN (100%) (100%) III stadium (>5 yrs) threatening DN (30%) (30%) IV stadium (>15 yrs) evident DN (25%) (25%) V stadium (>15 yrs) ESRD (20%) (20%)

Factors contributing to development of DN 1. Long-lasting hyperglycemia 2. Family predisposition 3. HT 4. High-protein diet 5. Cigarette smoking 6. hyperlipidaemia

BP in children of DM patients without DN with DN SBP mmHg mmHg Strojek i wsp. Mutual coincidence of DM and HT

DM patients with HT  Age of DM patients = % of patients with HT

BP, DM control and loss of GFR [ml/min/r] MABP [mm Hg] HbA1c <9% 1,41,53,64,46,0 HbA1c >9% 3,33,54,66,17,5

Treatment of DN 1. Proper treatment of DM 2. Proper treatment of HT 3. Quit smoking habit 4. Control of protein content in diet 5. Early treatment of anaemia 6. Early kidney replacement therapy

Proper treatment of DM 1. „Almost normal” glycaemia: fasting 60 – 140 mg/dl 2 h after meal <200 mg/dl 2. Proper body mass 3. Correction of hyperlipidaemia

Proper treatment of BP 1. Lowest tolerable BP 2. Treatement with ACE-I & AT-II

Nutrition state (albuminaemia) and the risk of death Hakim1994

Early treatment of anaemia with epo Anaemia… when? glomerulonephritis DN glomerulonephritis DN GFR <25-30 ml/min <35-40 ml/min creatinine >3-4 mg/dl>2-3 mg/dl Attention: ACE-I may contribute to anaemia!

Early start of renal replacement therapy 1. creatinine >3,5 – 4 mg/dl – a-v fistula! 2. creatinine >4,5 – 5 mg/dl (GFR 4,5 – 5 mg/dl (GFR <20 ml/min):- consider KTx (<45 yrs & IDDM) - consider KTx and pancreas Tx (>45 yrs & NIDDM) - start RRT

HD therapy in DM patients Pro: Contra: High efficiacy CVS damage Frequent control problems with a-v fistula No protein loss Hypotonia frequent hypoglycaemia frequent hyperkalaemia

CADO treatment in DM patients Pro: Contra: CVS neutral risk of infection No a-v protein loss Good control of kalaemiahernias Good control of glycaemiahelper required

Glycaemia regulation in DM patients with ESRD 1. Gluconeogenesis decreased by 30 – 40% 2. Insulin requirement decreased 3-4x 3. Decreased metabolism of some oral drugs (eg. metformin) 4. During HD glucose is „hemodialysed” and lost All the above may lead to hypoglycaemia!

DM patient on HD therapy- what should be the treatment? 1. Insulin – 2-3x lower doses! 2. Oral drugs – short acting, metabolized in liver eg: - glipizyd (Glipizyd, Minidiab, Glibenese GITS) - gliclazyd (Diaprel, Diabezyd) - glikwidon (Glurenorm)