Diabetes mellitus (DM) is a growing epidemic and is the most common cause of chronic renal disease (ERC) and renal failure.Diabetic nephropathy affects approximately 20 to 40% of diabetics and is one of the most common complications of DM.The detection of diabetic nephropathy together with early intervention is essential to delay its progression, accompanying adequate glycemic control.
Given the growing population currently affected by the DM, and therefore by nephropathy, it is very important to know the safe use of various hypoglycemicians in patients with nephropathy.On the other hand, it is essential to try to modify the risk factors of cardiovascular disease.In general, knowledge about the prevention and management of diabetic nephropathy along with other aspects of the care of the DM is part of the integral care of any diabetic patient.
review
Recommendations for the detection of nephropathy in diabetics
Studies for the detection of nephropathy in patients with DM should be done annually.In people with type 1 DM (DM1), the screening of nephropathy must begin 5 years after that diagnosis, since the moment of its beginning is known and microvascular complications take about 5 years to develop.On the other hand, in patients with type 2 DM (DM12), the screening should begin by diagnosing DM since the beginning of this type of DM is unknown.
Diabetic nephropathy can be detected by measuring albuminuria or creatininemia;Both tests must be carried out at least 1 time per year;Those with abnormal levels should repeat the analysis more frequently.Generally, in the first stage of nephropathy, high urinary albumin appears, which predicts the development of ERC and a gradual decrease in the glomerular filtering index (IFG).However, some individuals with ERC do not present initial high albuminuria.Therefore, it is important to perform the corresponding blood and urinary detection tests.These analyzes allow to identify more cases of nephropathy than the use of any of the solo tests.
Urinary albumin-creatinine ratio can be measured in an insulated urine sample or 4 or 24 hours.Microalbuminuria is defined as & GT; 30 mg/g of creatinine or 30 mg in 24 hours.The clinical macroalbuminuria is defined as & GT; 300 mg/g of creatinine or 300 mg in 24 hours.An abnormal value must be confirmed in at least another additional sample of urine, in a period of 6 months.Recently the terms "moderately augmented albuminuria" and "severely increased albuminuria" have been introduced.
The increase in albumin excretion is not only a marker of early diabetic renal disease but also of a higher risk of macrovascular disease.It is necessary to consider other causes of proteinuria such as infection, vigorous exercise, hypertension, heart failure and hematuria.Creatininemia serves to estimate IFG and, therefore, the degree of ERC.
"In an individual who presents nephropathy but no retinopathy other causes must be investigated."
It should also be considered that the development of nephropathy may not be related to diabetes itself.In patients with DM1, the appearance of retinopathy usually precedes the development of nephropathy.In an individual who presents nephropathy but no retinopathy other causes must be investigated.When the cause is uncertain, the patient must be referred to a nephrologist.Nephrologists can also help treat the complications of the progression of kidney disease, such as hypertension of difficult control, hyperkalemia and rapid progression.
glycemic control in chronic kidney disease
HeGlycemic control is essential to delay the appearance of DM complications, and can still be a challenge for the most experienced doctors.The glycemia control in patients with ERC adds another level of complexity.Detailed knowledge of what medications that can be used safely and how renal disease affects the metabolism of these medications is required.On the other hand, in each patient the objective glycemia should be established, recognizing that it can be difficult to interpret the data in the presence of kidney disease.
Glycemic target to achieve an A1c ~ 7.0%
Glycemic control is essential to delay or prevent nephropathy.In general, the A1C Objective recommended by the American Diabetes Association (ADA) for diabetes control is ≤7%.For certain populations, the ADA recommends higher figures (& lt; 8%) or stricter (& lt; 6.5%).
The American Association of Clinical Endocrinologists suggests an objective of the A1C ≤6.5% in patients who have a low risk of hypoglycemia, but also recognizes that the objectives should be individualized.
In 2007, the Kidney Disease Outcomes Quality Initiative guide for diabetes and ERC approves an A1C Objective & LT; 7.0%, but once the guide in 2012 is updated, the recommendation is 7.0%.
For DM1, many studies show that the development of microalbuminuria is associated with bad glycemic control.In control and complications trial (DCCT) diabetes, the intensive treatment of patients with DM1 (A1C average 9.1% vs. 7.2%) reduced the appearance of microalbuminuria in 34% in the primary prevention group and a43% in secondary intervention (patients with complications at the beginning of the study);The risk of progression to clinical albuminuria was also observed.
To evaluate whether the risk of diabetic nephropathy persists in the long term the European Diploma in Intensive Care Medicine showed that in the initial intensive group there were fewer cases of new microalbuminuria and progression to albuminuria.In this long -term follow -up study of the original DCCT work groups, it was shown that intensive treatment resulted in a significant decrease in the development of IFG & LT; 60 ml/min/1.73 m2.
In patients with DM2, Kumamoto studies, the UK Prospective Diabetes Study (UKPDS) and the Affairs Cooperative veterans showed that with intensive glycemic control the nephropathy of recent start and the progression of nephropathy was reduced.
A systematic review and a meta -analysis of 7 essays evaluated intensive glucose control at the final points related to the kidney in patients with DM2 and found less risk of developing microalbuminuria and macroalbuminuria.Intensive control groups had a median A1C that from 6.4 to 7.4%.The difference from A1C between intensive control groups and control groups was 0.6 to 2.3%;4 of the studies showed a difference of A1C & GT; 1%.The analysis also found that there were no benefits in terms of duplication of serum creatinine, the development of terminal nephropathy or death related to kidney disease.
The ACCORD study showed greater risk of hypoglycemia and mortality in patients with DM2 treated with intensive glucose control (A1C average 6.4% vs. 7.5%), without any reduction in the risk of cardiovascular diseases.The increase in mortality could not be attributed to hypoglycemia.In the Advance test, the most intensive glycemia control (A1C 6.5% vs. 7.3%) showed no reduction in cardiovascular diseases.However, the intensive group had a reduction in 21%nephropathy.The AFFAIRS Trial veterans study (intensive group with A1C 6.9% vs. 8.4%) also did not find anyBenefit in the risk of cardiovascular disease with strict glucose control.
The data clearly shows that the reduction of the A1C leads to a benefit in regards to nephropathy.The benefits of A1C reduction are also seen in retinopathy and neuropathy rates.However, the effect of reducing the A1C is much less in regards to macrovascular disease.Therefore, it is reasonable that an A1c Objective ~ 7.0% offers an optimal risk with greater benefit for the relationship than a considerably lower A1c objective.
glycemic objective in chronic kidney disease
Low A1C levels are associated with a higher risk of hypoglycemia, so it is necessary to adapt the A1C Objectives parra each patient.The consequences of hypoglycemia, which in turn can cause lesions, myocardial infarction, seizures, stroke or death, are greater in fragile and elderly patients, with irregular eating habits, treated with insulin and sulfonylureas, and with ERC.For those with a shorter life expectancy, history of severe hypoglycemia or asymptomatic hypoglycemia, ERC and children, the objective figures for the A1C must be higher.
The controversies Conference on Diabetic Kidney Disease (DKD) (conference on disputes in diabetic renal disease), contained in the Kdigo guide addressed a series of issues related to diabetic nephropathy, including the appropriate objectives of glycemic control.There are sufficient data and essays in relation to the ideal objective of blood glucose in patients with ERC in stages ≥3.
A study showed that A1C & GT levels; 9% and & LT; 6.5% were associated with greater mortality in the presence of degree ERC ≥3 not dialysis dependent.Diabetics with terminal nephropathy benefit maintaining their A1C between 7 and 8%, since A1C & GT levels; 8% O & LT; 7% carry risks of increase in global death and for cardiovascular cause.A recent observation of patients participating in research studies and who initiated lower age (& lt; 60 years) had a worse survival with an A1C & GT; 8.5% compared to those with an A1C of 6.5 to 7 to 7, 4%;There was no difference in elderly patients.
precision of HBA1c
A1C hemoglobin can be inaccurate in some patients with kidney disease.The factors that contribute include anemia by reduction of the shelf life of red blood cells, hemolysis and iron deficiency;There may be a false increase in hemoglobin carbamylation levels and the presence of acidosis.Fructosamine and glycosylated albumin are alternative measures available to estimate glycemic control.
Fructosamine reflects the glycation of multiple serum proteins, while glycosylated albumin reflects only the glycation of albumin;Both provide an estimate of control in the last 2 weeks.It is not clear if for diabetics with ERC your measurement is superior to that of the A1C for glycemic control.
Some studies indicate that glycosylated albumin is higher than A1C in dialysis patients, since A1C tends to underestimate glycemic control in patients with terminal nephropathy, but others argue that A1C remains the gold standard for these patients.
Medical treatment of diabetic nephropathy
The medical treatment of the DM is continuously changing as new therapies and new knowledge about the safety profile of the available medications appear.
Insulin
"The decrease in renal function is associated with a longer life of the longest insulin and a decrease in the need for insulin"
Patients with progression to kidney disease haveGreater risk of hypoglycemia due to the decrease in insulin cleance and some medications used to treat DM, as well as the deterioration of renal gluconeogenesis due to the decrease in the kidney mass.The kidney is responsible for approximately 30 to 80% of insulin elimination;The decrease in renal function is associated with a longer life of the longest insulin and a decrease in the need for insulin, coinciding with the decrease in IFG.
All available insulin preparations can be used in patients with ERC, but there is no advice on the specific reduction of insulin dosage in these patients.To achieve the desired blood glucose levels, the type of insulin, the dose and the administration must adapt to each patient but be careful not to cause hypoglycemia.
A randomized study of hospitalized patients treated with insulin doses according to the patient's weight and administered in bolus to patients with an IFG & LT; 45 ml/min/1.73 m2 with 0.5U/kg body weight vs.0.25u/kg body weight showed a similar glycemic control, but a significantly lower number of hypoglycemia in the group with the lowest basal weight based.
The anologists of the fast action insulin, the aspartic, the LISPRO and the glulisine are absorbed faster and are ideal for the rapid correction of hyperglycemia or by when postprandial insulin is necessary;It is what resembles the physiological secretion of insulin.Its action begins at 5-15 min with a peak at 30-90 min and an average duration of 5 hours.Some studies have shown that the action of glulisine is a little longer than that of the other fast -acting insulins.
These insulins can be administered up to 15 min before eating.They are used in the "basal bolus therapy" also known as multiple daily injections, but is also administered in continuous subcutaneous injection or insulin pump.
Patients with ERC in stages 4-5 and those in dialytic treatment usually have some delay in gastric emptying;Postprandial rapid insulin may be useful to match the peak of insulin action with the time of the postprandial glycemia peak.In patients with nausea who can or do not know how much they will eat, it may be useful to apply fast postprandial insulin.Similarly, peritoneal dialysis patients obtain large amounts of calories from dialysis fluid and often eat less than expected, so that postprandial dosage can also be useful.
The short-acting insulin available is the regular crystalline, which has a start of action at 30-60 min, and its peak of action occurs at 2-3 hours;with a duration of up to 5-8 hours.Ideally, regular insulin must be administered 30 minutes before food.The main advantage of regular insulin is its lower cost compared to rapid action analogues.
The insulin of intermediate action available is isopane or NPH.It has a start of action at 2-4 hours, the peak concentration occurs at 4-10 hours and the duration of its action reaches 10 to 18 hours.To achieve adequate basal coverage, it is dosed 2 times per day.Its use can be limited by its very variable absorption.Its cost is similar to that of regular insulin.
The analogues of prolonged action insulin are glargine and detection.
Glargina has an action start at 2-4 hours, with a minimum peak and a duration of 20 to 24 hours;Usually, apply 1 time/day.A unique property of glargine is that it does not have a clear peak.Detemir insulin has a start of action at 1-3 hours, with a small peak at 6-8 hours and a duration ofThe action from 18 to 22 hours.
Detemir insulin is dosed 2 times/day to give adequate basal coverage in the DM1;In the DM2, it is sometimes enough to manage 1vez/day.There are several pre -en -insulin preparations that have a fixed percentage of intermediate, fast or short action insulins.Because they contain 2 combined insulins, they have two separate peaks.An example is the “70/30” insulin that has 70% insulin NPH and 30% regular insulin.These presentations are convenient for patients who should receive 2 daily doses, but offer less and more restrictions on the insulin degree.It should be administered during fixed hours and the patient must ingest consistent foods.
Sometimes, insulin 70/30 is useful in patients who receive probe food for 12 hours.All insulin is 100U, and is presented as 100u/ml.The exception is 500U insulin, which has 500 insulin/ml units and is only available as regular insulin.
The high concentration of the 500U insulin alters the properties of regular insulin so that its pharmacokinetic is different.It has a similar action close to 30 minutes, but the peak occurs at 4–8 hours and lasts 14–15 hours.It can be administered 30 minutes before meals, in 2-3 daily doses, without using basal insulin.Generally, it is used in patients with severe insulin resistance and can be used in subcutaneous injection or pump.
oral medications
Metformin
"Metformin should not be used when creatininemia ≥1.5 mg/dl in men and ≥1.4 mg/dl in women"
Metformin increases insulin sensitivity and decreases hepatic gluconeogenesis;In some patients it can cause weight loss.Reduce A1C by 1.0–2.0%.The most common collateral effects are diarrhea, meteorism and cramps.With prolonged use, vitamin B12 deficiency has been found.
The FDA reports that metformin should not be used when creatininemia ≥1.5 mg/dl in men and ≥1.4 mg/dl in women, or when creatinine cleance is diminished in people & GT; 80 years.Because metformin is eliminated by the kidney, this recommendation aims to reduce the risk of lactic acidosis even in individuals with a mild deterioration of renal function.However, the global incidence of metformin lactic acidosis is very low.
A review of 347 prospective works and Cohort Observation studies, from the Cochrane database.
In a study that evaluated lactic acidosis associated with metformin in 14 patients, other causes of lactic acidosis (eg, clinical shock or tissue hypoxia) were identified, which were identified as the main cause and not specifically metformin;10 of these patients had an accumulation of metformin due to high creatininemia (3.05-11.8 mg/dl) while 4 patients with lower creatinemias and IFG still reduced did not have signs of accumulation of metformin.
Given the differences in creatinine translation in creatinine cleance on the basis of age, weight and race, it is reasonable to be guided by IFG and not by creatininemia alone.If the estimated IFG (IFGE) is & GT; 60 ml/min/1.73 m2, metformin can be used without reducing the dose.If the IFGE is ≥45-59 ml/min/1.73 m2, it is prudent to continue using metformin but adapting the dosage and with a narrower follow-up of the state of renal function (every 3 to 6 months).If the IFGE is ≥30-44 ml/min/1.73 m2, it is also necessary to have caution with the dosageAnd not to move from 1,000 mg/day or a 50%reduction, making renal function controls every 3 months and avoiding starting metformin in patients with this ERC level.
Metformin should be avoided with an ifge & lt; 30 ml/min/1.73 m2.It is recommended to suspend metformin in the presence of hypoxia situations or acute decrease in renal function, such as sepsis or shock, hypotension, acute myocardial infarction, and the use of radiographic contrast means or other nephrotoxic agents.This approach has been accepted by the various scientific societies including Kdigo and has been confirmed in additional studies.The DKD-KDIGO proposes to modify the recommendations of the FDA.
Sulfonylureas
Sulfonylureas bind to the sulfonylureas receiver in pancreatic ß cells and lead to an increase in insulin secretion.They descend the A1C by 1.5 to 2% and can cause hypoglycemia.First generation sulfonylureas are prescribed very little.Commonly, second generation sulfonylureas such as glipizide, glymepirid, glibrid and glyclazide are used.Sulfonylureas decrease A1C by 1-2%.
Sulfonylureas and their metabolites are eliminated by the kidney, which means that as IFG decreases the risk of hypoglycemia.The treatment with glymepirid and glibrid of patients with an IFG & LT; 60 ml/min/1.73 m2 considerably increases the risk of hypoglycemia, due to the presence of 2 active metabolites that are partly eliminated by the kidney.Gliburid should be avoided in patients with an IFGE & LT; 60 ml/min/1.73 m2.The glymepirid should be used with caution if the IFGE is & lt; 60 ml/min/1.73 m2 and is contraindicated in the presence of ifge & lt; 30 ml/min/1.73 m2.Less than 10% of the glipizide is eliminated by kidney but the same must be careful if the IFGE is & lt; 30 ml/min/1.73 m2 due to the risk of hypoglycemia.
Glinids
Natleglinida and rephakardidal as well as sulfonylureas increase insulin secretion by closing a sulfonylurea receptor and K -dependent channels of the ATP in pancreatic ß cells.They have a shorter half -life compared to sulfonylureas.They give rise to a rapid and short -term insulin release and should be taken before meals.They can also cause hypoglycemia.
Glinids reduce A1C by an average of 0.5 to 1.5%.In the ERC, the active metabolite of Natleglinida accumulates;Natleglinida should not be used with an IFGE & LT; 60 ml/min/1.73 m2.The active metabolite of Natleglinide is refined by hemodialysis, therefore it can be used in patients under dialysis.Conversely, the repair seems to be safe in individuals with ERC.However, it is reasonable to be cautious in patients with more serious renal dysfunction, with ifge & lt; 30 ml/min/1.73 m2, and start with the lowest dose (0.5 mg) to slowly increase.
Tiazolidinadionas
Tiazolidinadionas (pioglitazone, rosiglitazone) increase insulin sensitivity by acting as PPAR agonists (receptors activated by peroxidase proliferator).They do not cause hypoglycemia and decrease the A1C between 0.5 and 1.4%.They are metabolized by the liver and can be used in ERC.
However, an important limiting side effect is fluid retention and should not be used in advanced heart failure.This also makes its use limited in the ERC, in particular the patients is on dialysis.These drugs have been related to an increase in fracture and bone loss rates, therefore their use should be considered in patients with underlying bone disease (such as renal osteodystrophy).Before any degree of ERC it is necessary to adjust the doses.
In September 2010, the FDA restricted theUse of the Rosiglitazone because some studies related it with greater a higher number of cardiovascular events but in 2014, after other investigations, these restrictions were raised.
It has been proposed that there is an association between pioglitazone and bladder cancer, but this could not be confirmed in the relevant investigations.Recently, a combined analysis of several populations also did not find any association between thiazolidinadionas and bladder cancer.
Α-glucosidase inhibitors
The α-glucosidase inhibitors (carbose, miglitol) decrease the rupture of oligosaccharides and disaccharides in the small intestine, decreasing the intake of carbohydrates and delaying the absorption of glucose after food.The most important side effect is abdominal distention, flatulence and abdominal cramps.They normally reduce the A1C by 0.5 to 0.8% and in general do not modify the weight.
The caress is absorbed very little;In the urine only & lt appears; 2% of the drug and its active metabolites.If the renal function is reduced, serum carrbitation levels and their metabolites are significantly higher.Miglitol has greater systemic absorption and & GT; 95% is excreted by urine.It is recommended to avoid its use in patients with an IFG & LT; 25 ml/min/1.73 m2.On the other hand, no studies have been done on their long -term administration in patients with a creatinine & GT; 2 mg/dl, so their use should be avoided in these patients.
Dipeptidil peptidase-4 inhibitors
Peptidase 4 (DPP 4) dipeptidyl inhibitors decrease the decomposition of incredine hormones, such as LPG-1, and are sitegogtin, saxagliptine, linagliptin and alogliptin.These medications do not modify the weight and decrease the A1C by 0.5 to 0.8%.
Approximately 80% of the sigliptin is eliminated by the kidney.With an IFGE ≥30 a & lt; 50 ml/min/1.73 m2 the 50 mg dose should be used, 1 time/day, while with an ifge & lt; 30 ml/min/1.73 m2 it is advisable to useThe 25 mg dose, 1 time/day.
Saxagliptin also needs to be reduced to 2.5 mg/day if IFGE is ≤50 ml/min/1.73 m2;On the contrary, the standard dose for an IFGE & GT; 50 ml/min/1.73 m2 is 2.5 or 5 mg/day.Only a small amount of linagliptin is eliminated by urine;Therefore, although the IFG is reduced, it is not necessary to adjust the doses.If the IFGE is & lt; 60 ml/min/, 73 m2, the dose of alogliptin also needs to be adjusted, based on a baseline dose of 25 mg/day, at 12.5 mg/day.If the IFGE is & lt; 30 ml/min/, 73 m2, the dose should be 6.25 mg/day.
Sodium-Glucose Cotransporter inhibitors 2 (SGLT2)
SGLT2 inhibitors reduce glucose absorption at the renal level, causing an increase in glucose excretion and a A1C reduction of 0.9–1.0%.Augmented glucosuria can cause weight loss of up to 5 kg in 1 year.Due to the increase in adverse events related to the contraction of cardiovascular volume, in patients with an IFGE of 45 A & LT; 60 ml/min/1.73 m2, Canagliflozine should not be administered in doses & GT; 100 mg, 1 time/day.On the other hand, it should not be used if the IFGE is & lt; 45 ml/min/1.73 m2, due to adverse effects and their lower efficacy.The Dapagliflozine is not indicated if the IFGE is & lt; 60 ml/min/1.73 m2 but the wallpaper can be used even if the IFGE is & lt; 45 ml/min/1.73 m2.
Other oral medications
Bromocriptine (dopamine receiver agonist) has been properly studied in ERC.
Colsevelam (a bile acid kidnapping) does not show differences in its efficacy and safety in patients with an IFGE & LT; 50 ml/min/1.73 m2 but the data is limited to the most serious ERC.
Other subcutaneous medications Glucagon 1 (LP-1) peptide receptor agonists (LPG)
Exenatida (prolonged and regular liberation) and liraglutida are injectable medications that mimic intestinal hormones known as incredine, which lead to insulin release, and retard glucagon secretion and gastric emptying.They are approved by the FDA to be used with metformin and/or sulfonylureas, although in practice they are also used with insulin.
They contribute to central satiety thus reducing appetite and, often, also weight.The average A1C decrease is 0.5-1.0%.Both agents have associated with pancreatitis, while nausea is a common side effect that can limit its use.On the other hand, in animal studies, liraglutida has been associated with the development of C cell thyroid tumors and therefore should not be prescribed to patients with a risk of thyroid spinal cancer.The exenatida is administered 2 times/day and the liraglutida, 1 time/day;The ex -release of prolonged liberation is applied 1 time/week.The albigliutida and the doraza are other agonists of the LPG-1 receiver that can also be dosing 1 time/weekly.
The elimination of exenatida decreases as the IFG is lower.On the other hand, in a clinical case of a patient with renal insufficiency and ERC, the use of the exenatida produced an increase in creatininemia that was resolved by suspending the medication.The FDA reported cases of acute renal failure associated with the use of the exenatid/min/1.73 m2.
The main metabolization site of the liraglutida is not the kidney and therefore it is not necessary to adjust the dose in patients with renal failure, even without they are in the terminal stage of nephropathy, although the data in this population are limited.If the IFG is diminished, it is also not necessary to adjust the doses of albiglutida or Dreamaglutide.The manufacturer has reported cases of renal failure and worsening of chronic renal failure associated with the use of these drugs and advises to have caution when starting or increase the dose in patients with nephropathy.
Amiline analogues
Pramlintida is an injectable medication that is used with meals as a complement to insulin therapy, both in DM1 and DM2.Amiline is secreted together with insulin by pancreatic ß cells and their levels are low in diabetics.It usually reduces A1C by 0.5 1.0%.It seems that in ERC it is necessary to adjust the dose but has not been studied in terminal nephropathy.
Strategies for the control of glycemia and other risk factors
The main objective of optimizing glycemic control to reduce the development of microvascular and macrovascular complications is universal.The medication regime is done according to the patient's comfort and the doctor and must be personalized, especially because of the changes in renal function.Commonly, for those who need insulin, multiple daily injections are used to an average of 4/day.
The closest approach to the secretion of physiological insulin that can be achieved is through continuous subcutaneous infusion with an insulin pump.In the pump a single type of insulin is used, as a rapid action analogue, which serves as a basal bolus and correction insulin.Insulin pumps require surveillance by the patient and their use must be supervised by the endocrinologist and experienced educators.
There are continuous glucose monitoring systems that allow to measure blood glucose: a small plastic catheter is inserted subcutaneously and measured theglucose every 5 minutes.Patients can see this in real time and detect increases or decreases in glucose The additional benefit is that high and low readings can be adjusted.
In addition to blood glucose control, a comprehensive patient care approach must be advised.For weight control, the modification of behavior and lifestyle modifications, nutrition improvement, modification of food intake and glycemia monitoring are important.
For the treatment of nephropathy it is necessary to make adequate modifications, with the nephrologist's advice.Control of blood pressure should also be done.In itself, DM is an important cause of cardiovascular diseases and individuals with ERC usually die from cardiovascular diseases, the same being the main cause of death in this population.The presence of microalbuminuria, albuminuria and decrease in IFG are known predictors of cardiovascular disease.
The combination of DM and ERC is especially powerful in terms of the risk of cardiovascular disease, which requires a very narrow control of risk factors.In addition, control of hypertension, dyslipidemia and weight should be addressed.Nutrition represents an important role in diabetics with kidney disease;There must be a balance of the different dietary factors, including NA, K and P, while protein intake, carbohydrates and unhealthy fats should also be controlled.
In general, in overweight and obesity patients it is recommended to lose weight and increase exercise, taking into account the need to do heart stress tests.It is useful to resort to an experienced dietitist and a certified diabetes educator to properly follow a safe diet, the exercise plan and achieve the objective weight.The DKD-KDIGO addresses some of the issues related to the management of diabetic nephropathy, including dyslipidemia management and blood pressure control.The American Association of Diabetes also makes recommendations on the management of blood pressure and dyslipidemia.
Medical treatment in patients on dialysis and post -transplant
There are a few oral agents that can be used safely in dialysis patients, especially if DM is quite mild.However, most other patients will need insulin for glycemic control.Hemodialysis patients can have different insulin elimination rates, which may be affected by dialysis.The authors have done continuous control of glucose in patients in hemodialysis and found that glycemic responses are quite idiosyncratic so they consider that insulin regimes should be customized, to avoid both hyper and hypoglycemia during and after hemodialysis.
Peritoneal dialysis patients are exposed to large amounts of glucose in dialysis fluid, which can lead to non -controlled hyperglycemia.In continuous peritoneal dialysis patients it is better to use insulin in a standard or bolus regime.However, if a nightly dialysis night cycler is used, to better cover the increase in glucose load, it may be better to use a combination of insulins with fixed doses, such as insulins 70/30 or 75/25, administered at the beginning ofPeritoneal dialysis.Often, the nephrologist in charge of peritoneal dialysis modifies the glucose concentration of the dialysis fluid according to the need for greater or lesser removal of liquid and those changes must be coordinated with the endocrinologist so that insulin doses can be changedproperly.
In itImmediate period after transplantation, glycemic control can decline acute due to the initiation of anti -rejection treatment (glucocorticoids, calcineurin inhibitors, sirolimus) and increased insulin resistance.On the other hand, patients may experience other fluctuations in their daily routines such as diet adjustments, activity and medications.Because there are many variables present, glycemic control can fluctuate a lot, which requires strict blood glucose control and medication adjustment.
Conclusions
The management of patients with DM and nephropathy needs to take into account several aspects.Personalized glycemia control is important to achieve the necessary control to reduce complications, but safely, monitored.
Nephropathy development detection should be done regularly to identify microalbuminuria or IFG reductions, as well as establish a personalized regime.
The prevention and treatment of diabetic nephropathy and other complications need a multifactorial approach with the intervention of diabetologists, nephrologists, dietitians, diabetes educators and other specialists in diabetes complications, to provide a multifaceted care program and be able to reduce progressionof the disease.
Translation and Summary Objective: Dr. Marta Papponetti
