Medlemstidning för Svensk Förening för Diabetologi Aktuell Info för medlemmar

Proteinuria and Progressive Renal Disease
(Towards Preventing Renal Disease) in Diabetes Mellitus
Fourth International Symposium Switzerland, September 1997 Organisers: M Burnier (Switzerland), G Boner (Israel), H Brunner (Switzerland), D van Dijk (Israel), A Donker (The Netherlands), CE Mogensen (Denmark)

This item will concentrate particularly on the session Status on microalbuminuria - diabetes, Type 1 and 2 intervention studies: with focus on ACE inhibition session. Whilst the programme also looked at alternative interventions, these were mainly newer, putative agents for the treatment of diabetic kidney disease with angiotensin II inhibition, advanced glycation inhibition, transforming growth factor beta inhibition and the beta isoform of protein kinase C inhibition being discussed.

Comment G Boner, Tel Aviv University, Israel Describing the several guidelines published regarding the optimal treatment for patients with diabetic nephropathy, Professor Boner struck a warning note on behalf of the patient.1-6

It has become apparent that, unfortunately, most patients, do not receive optimal treatment, with the guidelines for the care of the hypertensive and diabetic patient not being followed by a substantial proportion of primary care and hospital physicians. The challenge, as outlined by Professor Boner, is to agree clear guidelines for the care of the non-diabetic renal patient, and to then improve the care of patients with diabetic and non-diabetic renal disease by establishing special clinics and by the education of the primary physician.

ACE inhibitors for protection against microvascular complications in patients with Type 1 diabetes N Chaturvedi, University College London, UK
Dr Chaturvedi discussed the results of the EUCLID (EUrodiab Controlled trial of Lisinopril in Insulin-dependent Diabetes) study, a randomised, double-blind, placebo-controlled trial of the effect of lisinopril on urinary albumin excretion rate (AER) and the progression of retinopathy in normotensive insulin-dependent diabetic patients with normoalbuminuria or microalbuminuria. Both normotensive and hypertensive microalbuminuric diabetic patients benefit from the use of angiotensin converting enzyme (ACE) inhibitors; it might also be that normoalbuminuric patients would also benefit from ACE inhibitors, and so Dr Chaturvedi specifically wanted to address the question as to when ACE inhibitors should be used in Type 1 (insulin-dependent) diabetic patients.

Five-hundred and thirty patients, aged between 20 and 59 years of age, with Type 1 diabetes with normoalbuminuria (AER <20 mcg/min) or microalbuminuria (AER 20-200 mcg/min) were recruited from 18 European centres. None of the patients were receiving medication for hypertension (resting blood pressure between 75 and 90 mmHg diastolic, and <=155 mmHg systolic). Patients were randomised to receive either lisinopril (10-20 mg daily) or placebo.

Effect of lisinopril on AER
AER was assessed by two overnight urine collections at baseline, 6, 12, 18 and 24 months. Retinal photographswere taken at entry and 24 months (n=354) and graded into 5 groups (no retinopathy to proliferative retinopathy).

After 2 years, lisinopril had significantly reduced AER by 18.8% (95% CI 2.0, 32.7; p=0.03) adjusted for baseline AER and centre (compared with placebo), with an absolute treatment difference of 2.2 mcg/min (against a mean AER of about 8 mcg/min). In normoalbuminuric patients the treatment difference was 12.7%, with an absolute treatment difference of 1.0 mcg/min (p=0.10), whilst in those with microalbuminuria the difference was 49.7% with an absolute difference of 38.5 mcg/min (p=0.04). Within the normoalbuminuric group, looking at the relative treatment effects at the end of the study in patients with different AERs at baseline (i.e. <5 mcg/min; 5-<10 mcg/min; 10-<20 mcg/min; 20-200 mcg/min) Dr Chaturvedi highlighted that there was a substantial treatment effect in patients with AERs not considered to be in the microalbuminuric range (i.e. a relative 20% difference [lisinopril vs placebo] in AER in the mid-range patients [5-<10 mcg/min AER; 10-<20 mcg/min]) and a 50% difference in favour of lisinopril in the 20-200 mcg/min AER group. It was only in the lowest baseline AER group (<5 mcg/min AER) that there was not much of an effect with lisinopril (5% difference lisinopril vs placebo). Thus, treatment with lisinopril slows the progression of renal disease in normotensive Type 1 diabetic patients with little or no microalbuminuria, with the greatest effect being seen in those patients not considered to be in the conventional microalbuminuric range (AER >= 20 mcg/min).

Effect of lisinopril on retinopathy.
Over the course of the 2-year study, retinopathy progressed by at least one stage in 13% of the lisinopril group compared with 23% of the placebo group (p=0.02). Lisinopril also tended to reduce the incidence of new retinopathy (OR 0.69; p=0.4) and progression to proliferative retinopathy (OR 0.18; p=0.03). In summary, Dr Chaturvedi felt that ACE inhibitors should be considered in the early stages of Type 1 diabetes.

Early intervention in microalbuminuria: 24-hour blood pressure and exercise changesPE Poulsen, E Ebbehøj, CE Mogensen, Aarhus University Hospital, Denmark In this session Dr Poulsen continued the theme of early intervention with ACE inhibitors. By the microalbuminuric stage, substantial pathophysiological changes have already taken place; blood pressure is elevated with an attenuated circadian rhythm and vagal function is impaired. In addition, there are abnormalities in kidney ultrastructure in Type 1 diabetic patients with microalbuminuria.

Dr Poulsen presented data from two randomised, placebo-controlled studies which looked at the effects of 2 years' treatment with lisinopril (20 mg) or placebo in normotensive, microalbuminuric Type 1 diabeticpatients. The first was a post hoc analysis of a subgroup of 60 patients with an AER between 20-70 mcg/min. In this study lisinopril significantly reduced AER compared with placebo (lisinopril baseline 35.5 mcg/min; 2 years 29.8 mcg/min: placebo baseline 36.3 mcg/min; 2 years58.8 mcg/min) and reversed the microalbuminuria to normoalbuminuria in 22 (69%) patients compared with 6 (21%) patients in the placebo group.

The second study was an examination of a subgroup of 22 patients in whom 24-hour ambulatory blood pressure (ABP), renal function and exercise-induced albuminuria were assessed. Over 2 years there was a small increase in ABP in the placebo group as opposed to significant reductions in the lisinopril group. There were no differences in glomerular filtration rate (GFR) or renal plasma flow in the two groups, but changes in AER and filtration fraction (FF) were positively correlated in the intervention group (r=0.9; p>0.01). Thus, the patients who showed the greatest fall in AER were also the individuals with the greatest fall in FF. Finally, in the lisinopril group, exercise-induced albuminuria developed at a slower rate compared with the placebo group,although this difference was not statistically significant. Dr Poulsen concluded that, in patients with low-grade albuminuria, treatment with an ACE inhibitor:
* reduces ABP without attenuating diurnal blood pressure variation;
* significantly reduces AER (with these changes being strongly associated with changes in FF);
* reverses microalbuminuria to normoalbuminuria in a significant proportion of patients compared with placebo.

Progression of renal disease B Brenner, Brigham and Women's Hospital, Boston, MA, USA
Dr Brenner stated that glomerular hypertension has been implicated as a major factor in mediating progressive renal damage after a number of initiating injuries. Amelioration of glomerular hypertension by dietary protein restriction or antihypertensive therapy reduces progressive glomerular damage in animals, these being the principal therapeutic interventions tested so far in patients. Glomerular hypertension and hyperfiltration also occur in humans with diabetes mellitus. Thus, dietaryprotein restriction would seem to delay the onset of end-stage renal disease as well as retarding the progression of diabetic renal disease. Citing the Modification of Diet in Renal Disease Study, Dr Brenner stated that dietary protein restriction, in combination with aggressive reduction in blood pressure, reduces the rate of progression of chronic renal disease in humans with significant proteinuria and baseline ongoing deterioration of renal function. ACE inhibitors have also been shown to offer protection in patients with diabetic and non-diabetic chronic renal disease. Indeed, evidence in support of a strong renoprotective effect of ACE inhibitors has been obtained in patients with overt nephropathy as well as in those with incipient nephropathy. Based on these findings various professional organisations have issued formal guidelines "enthusiastically supporting ACE inhibitors in diabetic subjects".1-3 In the same session, Dr Feldt-Rasmussen (Denmark) explained that microalbuminuria is present when the AER in a 24-hour urine, or in a shorter day-time collection, is in the range of 30-3000 mg/24 h (20-200 mcg/min equivalent to 0.46-4.6 mcmol/24 h). An AER in the microalbuminuric range is a strong predictor of nephropathy in Type 1 diabetes. However, despite the close relationship between microalbuminuria and diabetic nephropathy, kidney function in terms of GFR declines when AER is in the high microalbuminuric range.

Microalbuminuria has been shown to be an independent risk factor, not only of renal disease but also of cardiovascular disease, in both Type 1 and Type 2 (non-insulin-dependent) diabetic patients.

Detecting the risk of renal and cardiovascular disease in diabetes GC Viberti, Guy's Hospital, London, UK
In the first presentation in the Status of microalbuminuria session, Dr Viberti reinforced the importance of microalbuminuria as one of the strongest predictors for renal disease in Type 1 and Type 2 diabetes: for example, Type 2 diabetic patients with microalbuminuria had a much higher likelihood of early death, usually through coronary heart disease (50% over 7 years) compared with those patients with a normal AER. He emphasised that screening for microalbuminuria should be routine in diabetic patients.

Antihypertensive treatment in microalbuminuric Type 2 diabetic patients JCN Chan, Prince of Wales Hospital, Shatin, Hong Kong
In this review, Dr Chan highlighted that aggressive control of blood pressure not only controls glycaemia and hyperlipidaemia in Type 2 diabetics, but also reduces the rate of decline of renal function. She showed that although numerous antihypertensive agents have been shown to reduce blood pressure, and hence improve GFR, only ACE inhibitors are associated with anti-proteinuric effects which are independent of blood pressure reduction. In addition, ACE inhibitor therapy is associated with renoprotection in Type 1 and normotensive Type 2 diabetic patients with preserved renal function.

However, she stressed that diabetic patients often require multiple antihypertensive drug therapy, and that the optimal combination of these drugs has not yet been defined, although, at present, most people would advocate a combination of ACE inhibitor(s) and diuretics. In this regard Dr Chan showed follow-up data comparing the survival of patients who had been in a structured care programme within a clinical trial (i.e.optimal control of blood pressure, optimal control of liver glycaemia etc.) with those who had received a non-structured care programme. In a group of hypertensive, Type 2 diabetic patients, 8.2% of those who had received ACE inhibitors had died compared with 19.4% of those who had not received ACE inhibitors. These data suggest that patients do very much better within a controlled care programme which contains ACE inhibitor use. The effects of ACE inhibitors in diabetic patients with established renal disease (plasma creatinine >200 mcmol/l) require further investigation, since hyperkalaemia may be a concern in these patients.

Preservation of normal GFR in Type 1 diabetic patients with microalbuminuria under long-term (8 years') ACE inhibition E Mathiesen, E Hommel, HP Hansen, H-H Parving, Steno Diabetes Center, Gentofte, Denmark
This talk in the Status of microalbuminuria - diabetes, Type 1 and 2 intervention studies: with focus on ACE inhibition session was presented by Dr Mathiesen. This open, randomised, controlled study of 8 years duration has assessed the
long-term effectiveness of ACE inhibition on the preservation of GFR in Type 1 diabetic patients with microalbuminuria. Forty-four normotensive insulin-dependent patients with persistent microalbuminuria (AER 30-300 mg/24 h) were entered. The treatment group (n=21) received 50 mg bd captopril and low-dose thiazide, whilst the remaining patients (n=23) were left untreated unless hypertension developed (this occurred in 4 patients) with the aim of producing a difference in diastolic blood pressure between the 2 groups of 5 mmHg. Two patients from each group failed to complete the 8-year follow up. In the remaining patients, captopril treatment significantly reduced the progression of renal disease. From baseline to 8 years the fall in GFR was 12.2 ml/min (SE 6 ml/min; p<0.05) in the control group and 1.4 ml/min (2 ml/min; NS) in the captopril group. Forty per cent (9/23) of the control group patients compared with 10% (2/21) of the treatment group patients had progressed to nephropathy (p<0.02), with the control group reaching this end point earlier than the treatment group.

To investigate the effects of removing ACE inhibitor therapy, 16 treatment group patients and 2 control group patients were investigated before and 2 months after cessation of antihypertensive treatment. During this -month 'pause' in captopril treatment there was a significant increase in AER (p<0.001) and GFR (8.6 ml/min; SE 3 ml/min; p<0.01) with 6/16 (38%) of patients showing an AER above 300 mg/24 h. In the eight patients who had developed nephropathy, the fall in GFR was 25.6 ml/min (SE 10 ml/min; p<0.01) in the control group and -3.5 ml/min (SE 3 ml/min; NS) in the captopril group (p<0.01 between the groups).

Dr Mathiesen concluded that these results show that ACE inhibition postpones the development of diabeticnephropathy, an effect which is long lasting and associated with the preservation of normal GFR.

Long-term studies in Type 2 diabetes. Effects on nephropathy and retinopathy M Ravid, Tel Aviv University, Israel
Noting that ACE inhibitors are the preferred agents of choice of some researchers for renoprotection, Dr Ravid pointed out that other agents (such as calcium channel blockers and beta-blockers) show similar effects on the kidney. However, in the majority of cases the studies were short term and Dr Ravid felt that 4 years was not long enough to look at the effects of these agents. He felt that longer studies were needed.

Citing data from a 6-year study on the protective effects of ACE inhibitors in 156 normotensive-normoalbuminuric patients with Type 2 diabetes, who were randomised to receive placebo or enalapril, Dr Ravid showed that enalapril showed a modest but significant effect in attenuating the decline of creatinine clearance (mean decrease: placebo 2.5 ml/min/yr, enalapril 1.5 ml/min/yr; p=0.04) and on albuminuria (15/79 placebo patients vs 5/77 enalapril patients crossed the threshold to microalbuminuria; p=0.042). Diabetic retinopathy was recorded by an annual ophthalmoscopic examination, with 6% of new cases in the enalapril group vs 17% in the placebo group occurring during the course of the study. Combining these data with other data from a 5-year study of diabetics with microalbuminuria (7.8% of new cases in the enalapril vs 19% in the placebo group) gave a total of 2794 patient years of follow up. Here enalapril treatment resulted in an absolute risk reduction of 11.5 percentage points for the development of retinopathy (95% CI 6-27; p=0.024). Whilst cautioning against drawing conclusions from this highly selected, low-risk patient group and applying them to the diabetic population at large, Dr Ravid felt that these results suggested that very careful control of blood pressure at low normal levels carries an additional benefit for the prevention of nephropathy, and possibly also retinopathy, in low-risk, Type 2 diabetic patients.

ACE inhibition vs calcium channel blockade in normotensive Type 1 and Type 2 diabetic patients with microalbuminuria G Jerums on behalf of the Melbourne DiabeticNephropathy Study Group, Australia
Dr Jerums summarised the data from the Melbourne Nephropathy Study Group who investigated the relative effects of an ACE inhibitor with a calcium channel blocker. The results of the first study, a 12-month treatment with equihypotensive doses of perindopril or nifedipine (slow release) in Type 1 and Type 2 diabetic patients were presented in 1991, and showed that both treatments reduced AER in hypertensive patients and stabilised AER in normotensive patients. The second study (3-8 year follow up) in normoalbuminuric, Type 1 or Type 2 diabetics (who received placebo, perindopril or nifedipine) showed, at this interim stage, that in Type 2 patients:
* there were no effects of treatment on renal function (at a relatively short follow-up period);
* there was no change in mean blood pressure, but a significant lowering on 24-hour blood-pressure monitoring in favour of perindopril;
*there was a trend in albuminuria gradients (the nifedipine patients were stable, placebo patients rose and the perindopril patients had a lesser change).

In Type 1 patients, clinical blood pressures were not significantly different in the three treatment groups, again perindopril tended to lower the ABP and the trends in albuminuria showed that the perindopril group had a stable AER over 4 years, with the other two groups (especially nifedipine) showing upward trends. Reviewing the interim data from the two studies (perindopril vs nifedipine vs placebo), Dr Jerums felt that potentially there was no repression of albuminuria and no change in GFR in the Type 2 study, whereas in the Type 1 study there were changes in albuminuria without changes in GFR.

Long-term follow up of the GFR in normotensive Type 1 diabetic subjects with microalbuminuria during angiotensin I converting enzyme inhibition M Marre, P Fabbri, B Bouhanick, G Berrut, J-J Le Jeune, F Bled, Centre Hospitalier, Universitaire, Angers, France

Dr Marre reviewed the data from a prospective, open sequential, follow-up study of 25 normotensive Type 1 diabetic patients with microalbuminuria, 15 of whom received the ACE inhibitor enalapril as soon as microalbuminuria was identified (strategy 1), whilst the remaining 10 received enalapril only when they had progressed to macroalbuminuria (strategy 2). The patients were followed up at 4 years (range 24-72 months). At baseline six patients on strategy 1 had glomerular hyperfiltration and nine normofiltration, whilst in the strategy 2 group, three subjects had hyperfiltration and seven had normofiltration, meaning that there was no significant difference between the groups. At follow up, in the strategy 1 group, eight patients had hyperfiltration and seven normofiltration whereas in the strategy 2 group, one subject had hyperfiltration, four normofiltration and five hypofiltration (p < 0.01). The median rate of change in the GFR was 0.03 ml/min/1.73 m2/month (strategy 1) vs -0.86 ml/min/1.73 m2/month (strategy 2) [p=0.0016]. These results were considered attributable to the enalapril treatment strategy, but not to changes in blood pressure or to final status of AER. In conclusion, Dr Marre considered that the study showed that early treatment with enalapril (20 mg/24 h) prevents GFR declining in normotensive Type 1 diabetic patients with microalbuminuria.

Structural changes in microalbuminuria: effect of intervention R Østerby, Aarhus University Hospital, Denmark; HJ Bangstad, Aker University Hospital, Oslo, Norway; S Rudberg, Karolinska Instituttet, Stockholm, Sweden This presentation underlined the association between diabetes control, the development of structural changes in the kidney and concomitant changes in kidney function. Dr Østerby hoped that analysis of biopsies from a 3-year treatment with ACE inhibitors will show a demonstrable effect of ACE inhibitors on structural changes in the kidney. Furthermore, ongoing studies should clarify whether morphological studies are useful in intervention trials.


1.Viberti GC, Mogensen CE, Passa P, Bious R, Mangili R. St. Vincent Declaration, 1994. Guidelines for the prevention of diabetic renal failure. In: Mogensen CE (ed.) The Kidney and Hypertension in Diabetes Mellitus, 2nd ed. Kluwer 1994; pp 551-557.

2.Clark CM, Lee DA. Prevention and treatment of the complications of diabetes mellitus. N Engl J Med; 352: 1210-1217.

3.Bennett PH, Haffner S, Kasiske BL, et al.Screening and management of microalbuminuria in patients with diabetes mellitus: recommendations to the scientific advisory board of the National Kidney Foundation. Am J Kidney Dis 1995; 24:107-112.

4.Joint National Committee. The fifth report of the Joint National Committee on detection, evaluation and treatment of high blood pressure (JNC V). Arch Intern Med 1993; 153: 154-183.

5.National High Blood Pressure Education Program. National High Blood Pressure Education Program working group report on hypertension and chronic renal failure. Arch Intern Med 1991; 151: 1280-1287.

6.National High Blood Pressure Education Program. National High Blood Pressure Education Program working
group report on hypertension in diabetes. Hypertension 1994; 23: 145-1580.

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Typ II Diabetiker i dialys. En begynnande epidemi?

Soffía Gudbjörnsdottir, Göran Blohmé, Staffan Björck, Medicinkliniken och njurmedicin, Sahlgrenska Universitetsjukhuset, Göteborg.


Få områden inom den moderna medicinen kan redovisa så påtagliga framsteg som den utveckling som skett under de sista 15 åren när det gäller omhändertagandet av typ 1 diabetiker (ungdomsdiabetes) med njursjukdom. Från att ha varit en obönhörligt progressiv sjukdom som lett till död eller dialys/njurtransplantation hos de flesta patienter inom en tioårsperiod, kan sjukdomen fås att fortskrida mycket långsammare och njursvikt kan hos många patienter förhindras. Den överdödlighet som har konstaterats vid diabetes är huvudsakligen förknippad med utvecklingen av diabetisk njursjukdom (diabetesnefropati). Den betydande mortalitetsrisken som ses redan inom 10 år från debuten av njursjukdom har reducerats med ca 70% de sista 15 åren.

Trots dessa framsteg sker paradoxalt nog en ökning av antalet diabetiker i dialys i många länder. Diabetesnefropati har idag blivit den vanligaste orsaken till dialyskrävande uremi. Generellt sett ökar behovet av dialysresurser men diabetisk njursjukdom har i flera länder visat sig öka mer än övriga sjukdomar som orsak till dialyskrävande uremi. I USA har, under 10 års tid, andelen patienter med diabetesnefropati ökat från 30 till 40% av nyupptaget i dialys och samma utveckling finns rapporterat från Tyskland där man lokalt rapporterat upp till 44% diabetesnefropati i dialyspopulationen . Skälet till det är en ökning av typ 2 diabetes ("åldersdiabetes"), delvis beroende på en äldre befolkning. Sannolikt spelar också en ökad tillgänglighet av dialysresurser en roll samt att behandlingen förbättrats så att den kan tolereras även av sjukare patienter. Det skulle också kunna vara så att med bättre generellt omhändertagande överlever fler patienter fram till dialysstart. För att undersöka om vi är på väg mot en motsvarande utveckling i Sverige har vi analyserad nyupptaget i dialys av samtliga diabetiker i Göteborg.

Nyupptag i dialys bland diabetiker i Göteborg

Samtliga diabetiker identifierades som startat dialys i Göteborg sedan 1981 (1). Ålder, kön, andra sjukdomar och dialysform samt överlevnad registrerades. Sammanlagt 147 patienter startade dialys. 104 började med hemodialys och 43 med peritonealdialys (CAPD). Antalet diabetiker som startade dialys ökade från 11 de tre första åren till 45 de tre sista åren. Medelåldern för patienter som startade dialys ökade signifikant under observationstiden, från 41 år 1981 till 65 år vid slutet av 1996. Nyupptaget av patienter med diabetes i dialys som var yngre än 50 år var oförändrat under observationstiden medan nyupptaget av de som var äldre än 50 år ökade med 20% per år (figur 1). Genomsnittlig överlevnad i dialys var endast 1.6 år. Dödligheten hos diabetiker i dialys ökade under observationstiden men ökningen kan statistiskt förklaras helt av ökningen av äldre i dialys. Risken för död var 63% högre för patienter som startade dialys efter, jämfört med före 1990


Trots betydande framsteg när det gäller behandling ökar antalet diabetiker som startar dialys genom ett tillskott av äldre patienter. Det är sannolikt att behovet av dialysresurser för diabetiker kommer att öka. Redan idag torde kostnaden för dialys och transplantation för denna patientgrupp uppgå till ca 200 milj kr per år i Sverige. Övriga vårdkostnader för denna grupp är okänt men kan motsvara liknande belopp. Det är en alarmerande situation som kräver generella strategier som fokuserar på screening för njursjukdom och tidigt omhändertagande.

Diagnosen av diabetesnefropati är enkel och bygger på uppkomst av proteinuri hos patienter med diabetes ca 10-15 år efter diabetesdebuten i frånvaro av andra förklaringar. En albuminutsöndring i urinen av mer än 200 µg/minut fordras för diagnos. Vid typ 2 diabetes kan njursjukdom komma långt tidigare och ibland upptäckas i samband med diabetesdebuten. Numera kan proteinuri upptäckas tidigare genom känsligare metoder. En utsöndring av albumin i urinen över det normala men under vad som klassificerats som diabetesnefropati kallas mikroalbuminuri och denna fas kallas incipient eller begynnande nefropati. Tillståndet förutsäger med hög sannolikhet senare manifest njursjukdom och sjunkande njurfunktion. Gränsen sätts för närvarande till 20-200 µg/minut av albumin i urinen. Mätningen görs bäst i natturin för att undvika effekt av fysisk aktivitet. Två förhöjda prover av tre krävs för diagnos samt att annan förklaring inte föreligger (t.ex. urinvägsinfektion). Som screeningmetod duger stickprov på morgonurin där bara koncentrationen mäts men ett postitivt prov måste bekräftas med en kvantitativ metod.

Behandlingen av diabetesnefropati kan vara komplicerad och skall som regel ske av eller i samarbete med diabetologisk eller nefrologisk expertis när njurfunktionen är nedsatt. Behandlingen av diabetesnefropati syftar till att reducera de riskfaktorer som leder till försämring och där är förbättrad diabeteskontroll och blodtrycksbehandling de viktigaste komponenterna. Tidigare har inställningen till intensifierad diabetesbehandling i detta stadie varit passiv då man länge ansett att vinsten under denna fas varit liten men det är nu fastlagt att det aldrig är försent att förbättra diabeteskontrollen. Noggrann blodtrycksbehandling är sannolikt den viktigaste förklaringen till de prognosförbättringar som skett. Även om behandlingen är individuell är målet en normalisering av blodtrycket. Diuretikabehandling är en mycket viktig komponent eftersom diabetesnefropati alltid medför övervätskning. De sista åren har det visat sig att blodtrycksbehandling med ACE hämmare leder till särskilt kraftig minskning av proteinurin och dessa medel har blivit en av hörnstenarna i behandlingen tillsammans med diuretika. Graden av blodtryckskontroll är dock viktigare än vilket medel man använder. Det är möjligt att kolesterolsänkande behandling också skyddar njurfunktion varför kontroll av blodfetter är viktigt liksom rökstopp.

Med tanke på njursjukdomens allvarliga karaktär måste ett screeningprogram tillämpas, syftande till tidig upptäckt och intervention. Handläggning av tidigare stadier är en angelägenhet för alla som behandlar diabetiker. Det vidare förloppet och prognosen avgörs framförallt där patienten handläggs primärt, dvs som regel i primärvården. Socialstyrelsen har utarbetat nationella riktlinjer för diabetes. I detta ingår ett handlingsprogram för att omhänderta och förebygga njursjukdom vid diabetes som nära överensstämmer med internationella rekommendationer. Huvuddragen innebär att screening för microalbuminuri skall göras varje år hos alla patienter med diabetes upp till 70 års ålder. Förhöjda värden skall kontrolleras och om mikroalbuminuri kvarstår eller ökar skall detta betraktas som ett allvarligt tecken och leda till försök att förbättra glukoskontrollen. Om detta ej ger förbättring kan behandling med ACE-hämmare startas även vid normalt blodtryck och det har till och med rekommenderats att behandling skall ges vid mikroalbuminuri trots normal blodtryck där förbättrad sockerkontroll ej ger effekt. Vid blodtrycksbehandling är det svårt att generellt ange vilken nivå som skall eftersträvas och behandlingen måste individualiseras. Hos unga individer kan 125/80 mm Hg vara ett mål. Målet skall vara att stabilisera eller minska graden av albuminuri och bevara njurfunktion. Andra riskfaktorer som hyperlipidemi och rökning skall identifieras och behandlas.

Sammanfattningsvis är förbättrad diabeteskontroll den viktigaste primärpreventiva åtgärden och tidigt insatt och effektiv blodtrycksbehandling räddar njurfunktion och liv. Hur effektivt ett konsekvent screeningprogram är är svårt att bedöma men man kan konstatera att passivitet vid mikroalbuminuristadiet i de flesta fall leder till nefropatiutveckling. Ett aktivt förhållningssätt har bedömts som mycket kostnadseffektiv.


1 Gudbjörnsdottir S, Blohmé G, Björck S. Typ 2 diabetiker i dialys. En begynnande epidemi? Svenska Läkarsällskaoets handlingar. Hygiea, band 106, häfte 2, 1997.

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