Diabetic kidney disease in type 2 diabetes: a consensus statement from the Swiss Societies of Diabetes and Nephrology

DOI: https://doi.org/10.57187/smw.2023.40004

Anne Zanchiab, Andreas W. Jehlecd, Faiza Laminebe, Bruno Vogtf, Cecilia Czerlauf, Stefan Bilzg, Harald Seegerh, Sophie de Seigneuxi*

a Service of Nephrology and Hypertension, Department of Medicine, Lausanne University Hospital, Lausanne, Switzerland

b Service of Endocrinology, Diabetes and Metabolism, Department of Medicine, Lausanne University Hospital, Lausanne, Switzerland

c Department of Internal Medicine, Hirslanden Klinik St. Anna, Lucerne, Switzerland

d Transplantation Immunology and Nephrology, University Hospital Basel, Basel, Switzerland

e Unit of Diabetes and Endocrinology, Department of Internal Medicine, Riviera-Chablais Hospital (HRC), Rennaz, Switzerland

f Department of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Switzerland

g Internal Medicine and Endocrinology, Kantonsspital St Gallen, Switzerland

h Division of Nephrology, University Hospital Zurich, Switzerland

i Service of Nephrology and Hypertension, Department of Medicine, Geneva University Hospital, Switzerland

*Contributed equally

Anne Zanchi, MD

Service of Nephrology, Department of Medicine

Centre Hospitalier Universitaire Vaudois (CHUV)

Rue du Bugnon 17

CH-1011 Lausanne



Diabetic kidney disease is highly prevalent in patients with type 2 diabetes and is a major cause of end-stage renal disease in Switzerland. Patients with diabetic kidney disease are among the most complex patients in diabetes care. They require a multifactorial and multidisciplinary approach with the goal to slow the decline in glomerular filtration rate (GFR) and cardiovascular morbidity. With this consensus we propose an evidence-based guidance to health care providers involved in the care of type 2 diabetic patients with diabetic kidney disease.

First, there is a need to increase physician awareness and improve screening for diabetic kidney disease as early intervention may improve clinical outcomes and the financial burden. Evaluation of estimated GFR (eGFR) and spot urine albumin/creatinine ratio is recommended at least annually.

Once it is diagnosed, glucose control and optimisation of blood pressure control with renin-angiotensin system blockers have been recommended as mainstay management of diabetic kidney disease for more than 20 years. Recent, high quality randomised controlled trials have shown that sodium-glucose cotransporter-2 (SGLT2) inhibition slows eGFR decline and cardiovascular events beyond glucose control. Likewise, mineralocorticoid receptor antagonism with finerenone has cardiorenal protective effects in diabetic kidney disease. Glucagon-like peptide-1 (GLP1) receptor agonists improve weight loss if needed, and decrease albuminuria and cardiovascular morbidity. Lipid control is also important to decrease cardiovascular events. All these therapies are included in the treatment algorithms proposed in this consensus.

With advancing kidney failure, other challenges may rise, such as hyperkalaemia, anaemia and metabolic acidosis, as well as chronic kidney disease-mineral and bone disorder. These different topics and treatment strategies are discussed in this consensus. Finally, an update on diabetes management in renal replacement therapy such as haemodialysis, peritoneal dialysis and renal transplantation is provided.

With the recent developments of efficient therapies for diabetic kidney disease, it has become evident that a consensus document is necessary. We are optimistic that it will significantly contribute to a high-quality care for patients with diabetic kidney disease in Switzerland in the future.


For more than 20 years, the standard therapy of patients at risk of or with diabetic kidney disease included efficient glucose and blood pressure control and the use of renin-angiotensin system inhibitors. Although these therapies slow the decline in renal function, the number of patients with end-stage renal disease secondary to diabetes is still on the rise all around the world due to the high prevalence of diabetes, obesity and an aging population. Recently, large studies have demonstrated remarkable renal protective properties of new classes of drugs in type 2 diabetes. For this reason, prior recommendations published in this journal in 2014 need an update.

Patients with diabetic kidney disease are among the most complex patients in diabetes care. Their care is multifactorial and multidisciplinary, involving different groups of healthcare providers. The primary care physician, the diabetologist, the nephrologist, the nutritionist and the specialised nurse, among others, need to rely on a common view while treating these patients.

It has become evident that a consensus document is necessary to help all healthcare providers involved in the care of patients with diabetic kidney disease. With this consensus, we propose a concise document summarizing the important topics around diabetic kidney disease. It includes therapies with proven efficacy and which are available in Switzerland. It largely extends the document in 2014 endorsed by the Swiss Society of Endocrinology and Diabetes (SGED/SSED). This consensus will be updated yearly on its digital platform (diabetic kidney disease SSED/SGED (www.sgedssed.ch) and Swiss society of Nephrology (SSN) (www.swissnephrology.ch) guidelines; www.guidelines.ch).

The working group included diabetologists and nephrologists across Switzerland and extended between 2019 and 2022. Those participating in the workshop are co-authors of the consensus. Before its publication, it was reviewed by the Swiss Society of Endocrinology and Diabetes and by the Swiss Society of Nephrology. 

Definition of and screening for diabetic kidney disease

References for this section: [1–11]

Screening for diabetic kidney disease (DKD) is important because it is a silent disease and symptoms develop only at very late stages. Primary care physicians and endocrinologists remain central to the screening process. The yearly recommended screening of creatinine-based estimated glomerular filtration rate (eGFR) and urine albumin/-creatinine ratio has not changed for many decades and will identify patients with significant kidney disease. Yet the urine albumin/creatinine ratio is often lacking in the annual workup, as is the calculation of creatinine-based eGFR. Therefore, there is a constant need to improve physician awareness of diabetic kidney disease by implementing systematic screening and clear classification of patients with diabetes and nephropathy. New biomarkers identifying patients with early renal function decline are actively being investigated (such as tumour necrosis factor [TNF] receptors 1 and 2, kidney injury molecule-1 [KIM-1]). They will hopefully provide a tool for better stratification of patients and intervention in the early stages of diabetic kidney disease.

Epidemiology of diabetic kidney disease


Diabetic kidney disease 

Diabetic nephropathy 

Screening and KDIGO classification

Yearly screening in all (table 1).

Classification: KDIGO G1–5, A1–3 (table 1).

Expert opinion: dynamics over time are important to document as:

Table 1KDIGO 2012 classification and recommended frequency of monitoring per annum (modified from: Kidney Disease: Improving Global Outcomes (KDIGO) Diabetes Work Group. KDIGO 2020 Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease. Kidney Int. 2020 Oct;98(4S):S1-S115 [1]).

Guide to frequency of monitoring (number of times per year) by GFR and albuminuria category  Persistent albuminuria categories. Description and range 
A1  A2  A3 
Normal to mildly increased  Moderately increased  Severely increased 
<3 mg/mmol  3–30 mg/mmol  >30 mg/mmol 
GFR categories (ml/min/1.73 m2): description and range G1 Normal or high ≥90 1 if CKD 1 2
G2 Mildly decreased 60–89 1 if CKD 1 2
G3a Mildly to moderately decreased 45–59 1 2 3
G3b Moderately to severely decreased 30–44 2 3 3
G4 Severely decreased 15–29 3 3 4+
G5 Kidney failure <15 4+ 4+ 4+

GFR: glomerular filtration rate

Limitations of eGFR formulas

––Twenty-four-hour urine collection is only recommended in situations where creatinine values are less accurate in the estimation of GFR (see above). However it has several caveats (errors in urine collection, tubular creatinine secretion with declining renal function). 

Search for non-diabetic causes of nephropathy and criteria for referral to nephrologist

Blood glucose control and antidiabetic drugs in diabetic kidney disease

References for this section: [1, 2, 12–32] 

The 1990s demonstrated that tight glycaemic control prevents the early stages of diabetic kidney disease in type 1 diabetes (DCCT, EDIC), which was confirmed in type 2 diabetes later on. Recently, new classes of antidiabetic drugs have been proven to have powerful renal protective effects in type 2 diabetes, particularly the sodium-glucose cotransporter-2 (SGLT2) inhibitor class. Their effects are beyond glucose control, opening an exciting period in the field of chronic kidney disease. This section highlights the important facts around glycaemic control and antidiabetic drugs in diabetic kidney disease. For general information on antidiabetic therapy in type 2 diabetes, we refer to www.sgedssed.ch. Only frequently prescribed antidiabetic drugs are discussed.

Blood glucose control and diabetic kidney disease

Antidiabetic therapy and diabetic kidney disease

Figure 1 Adjustment of dosages according to eGFR (Swissmedic [Switzerland], for other countries refer to local restrictions).

Figure 2 Antidiabetic therapy in chronic kidney disease stage G1–3 A2–3 (modified from: Kidney Disease: Improving Global Outcomes (KDIGO) Diabetes Work Group. KDIGO 2020 Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease. Kidney Int. 2020 Oct;98(4S):S1-S115 [1]).

Per eGFR see figure 1.

Comment: dual SGLT2 inhibitor – GLP1 agonist therapy is under investigation. Preliminary results demonstrate additional effects on weight, blood glucose and blood pressure control.

SGLT2 inhibitor prescription in diabetic kidney disease

GLP1 receptor agonist prescription in diabetic kidney disease

Metformin prescription in diabetic kidney disease

DPP-IV inhibitor prescription in diabetic kidney disease

Sulphonylurea/glinide prescription in diabetic kidney disease

Insulin prescription in diabetic kidney disease

Blood glucose targets in chronic kidney disease

Blood pressure control and diabetic kidney disease

References for this section: [33–40] 

Hypertension and diabetes coexist in a vast majority of patients with type 2 diabetes. Antihypertensive therapy is beneficial for both cardiovascular and renal outcomes in patients with type 2 diabetes and is central to the standard of care in this population. The exact goal of blood pressure control remains unclear as studies with specific blood pressure goals in diabetic kidney disease are lacking. The UKPDS, HOT and ADVANCE BP trials, dedicated to patients with type 2 diabetes, failed to achieve a systolic blood pressure goal of <130 mm Hg. The ACCORD BP study showed no clear evidence that a systolic blood pressure goal of <120 mm Hg is beneficial for cardiovascular endpoints, except for stroke reduction and albuminuria progression with, however, more serious adverse events such as hypotension and hyperkalaemia. Thus, proposed goals are based on consensus statements and may differ from each other. A goal of <140/90 mm Hg has a high level of evidence for cardiac and renal protection whereas a goal <130 mm Hg has a high level of evidence for stroke reduction. The ADA 2021 guidelines recommend targets of <140/90 mm Hg in all or <130/80 mm Hg in those at higher cardiovascular risk (established or 10-year atherosclerotic cardiovascular disease [ASCVD] risk >15%). KDIGO 2021 guidelines recommend a systolic blood pressure goal of <120 mm Hg using standardized office blood pressure measurement in patients with chronic kidney disease, with or without diabetes, not undergoing dialysis. However, KDIGO acknowledge that the evidence supporting such a goal is less certain in diabetes.

Both angiotensin converting-enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) reduce the progression of albuminuria in diabetic kidney disease more effectively than other drug classes. The renal protective effects are beyond the blood pressure lowering effects. They are recommended as first line therapy (fig. 3).

Diagnosis of hypertension in diabetic kidney disease

Table 2Classification of office blood pressure* and definition of hypertension grade** (modified from: Williams B, et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. J Hypertens. 2018;36(10):1953–2041 [36]).

 Category  Systolic (mm Hg)  Diastolic (mm Hg) 
Optimal <120 and <80
Normal 120–129 and/or 80–84
High normal 130–139 and/or 85–89
Grade 1 hypertension 140–159 and/or 90–99
Grade 2 hypertension 160–179 and/or 100–109
Grade 3 hypertension ≥180 and/or ≥110
Isolated systolic hypertension ≥140 and <90

 * Blood pressure category is defined according to seated clinic measurement and by the highest level, whether systolic or diastolic.

** The same classification is used for all ages from 16 years.

Table 3Definition of hypertension according to office, ambulatory and home blood pressure levels (modified from Williams et al. J Hypertens. 2018;36:1953-2041 [36]).

 Category  Systolic (mm Hg)  Diastolic ( mm Hg) 
Office blood pressure*  ≥140 and/or ≥90
Ambulatory blood pressure Daytime (or awake) mean ≥135 and/or ≥85
Night-time (or asleep) mean ≥120 and/or ≥70
24-hour mean ≥130 and/or ≥80
Home blood pressure mean ≥135 and/or ≥85

* Refers to conventional office blood pressure rather than unattended office blood pressure

Table 4Office blood pressure treatment target ranges (modified from Williams et al. J Hypertens. 2018;36:1953-2041 [36]).

 Diabetes  CKD 
SBP Age 18–65 Target to 130 or lower if tolerated, not <120  Target 130–139 if tolerated 
Age ≥65 Target to 130–139 if tolerated  Target 130–139 if tolerated 
DBP 70–79 70–79

CKD: chronic kidney disease; DBP: diastolic blood pressure; SBP: systolic blood pressure

Figure 3 Proposed algorithm of blood pressure target and management in diabetic kidney disease.

Comments on blood pressure control in diabetic kidney disease

Mineralocorticoid receptor antagonism in diabetic kidney disease

References for this section: [41–45] 

The mineraolcorticoid receptor is an important contributor to the development of diabetic kidney disease. Mineralocorticoid receptor overactivation is assumed to promote kidney inflammation and fibrosis in diabetic individuals. The steroidal mineralocorticoid receptor antagonists (MRAs) spironolactone and eplerenone reduce albuminuria either as monotherapy or on top of ACE inhibitor or ARB treatment in diabetic kidney disease. They are also indicated for the treatment of HFrEF and refractory arterial hypertension. However, no studies examine the impact of steroidal MRA treatment on hard endpoints in diabetic kidney disease.

Finerenone, a specific and nonsteroidal MRA improves renal (–18%, number needed to treat [NNT] 29, p = 0.001) and cardiovascular outcomes (3PMACE+HHF, –14%, NNT 42, p = 0.03) if given in addition to maximum tolerated RAS blockade, with only a modest effect on blood pressure in patients with type two diabetes, proteinuric diabetic kidney disease and an eGFR of 25–75 ml/min/1.73m2. Treatment doubles the risk of hyperkalaemia. Only 4.6% of the patients were on an SGLT2 inhibitor, therefore the exact treatment effect of combination therapy is unclear. Also, no head-to-head comparisons of the cost-effectivenes of different MRAs exist. Post-hoc analyses suggest that the addition of finerenone to a SGLT2 inhibitor further reduces albuminuria. In addition, cardiorenal protection with finerenone appears to be independent of SGLT2 inhibitor use. Finally, the risk of hyperkalaemia was significantly lower with the SGLT2 inhibitor + finerenone combination.

Lipid control and diabetic kidney disease

References for this section: [46–57] 

Metabolic factors, among them dyslipidaemia and diabetes, are the most important modifiable cardiovascular risk factors and cardiovascular diseases are the most important causes of death in both patients with diabetes and patients with chronic kidney disease. Therefore, lipid-lowering treatment is among the cornerstones of cardiovascular disease prevention in both diabetes and chronic kidney disease. This has been adopted in recent guidelines, which uniformly advocate the use of lipid-lowering treatment, mostly statins, in patients with diabetes and chronic kidney disease not requiring dialysis.

Cardiovascular risk in chronic kidney disease

Table 5Current recommendations on cardiovascular risk stratification in diabetes and chronic kidney disease [51, 58].

EAS/ESC, 2021 Very high risk if Patients with DM with established ASCVD and/or severe target organ damage eGFR <45 ml/min/1.73 m2 irrespective of albuminuria
eGFR 45–59 ml/min/1.73 m2 and microalbuminuria (ACR 3–30 mg/mmol)
ACR >30 mg/mmol
Presence of microvascular disease in at least 3 sites (i.e., ACR >3 mg/mmol plus retinopathy plus neuropathy)
High risk if Patients with DM of >10 years duration or ≥1 CVD risk factor without ASCVD or target organ damage
Moderate risk if Patients with DM and none of the above

ACR: urinary albumin/creatinine ratio; ASCVD: atherosclerotic cardiovascular disease: DM: diabetes mellitus;

Dyslipidaemia in diabetic kidney disease

Lipid lowering therapy in diabetes and/or chronic kidney disease



PCSK9 inhibitors


Dyslipidaemia and cardiovascular risk in renal transplant recipients


Table 6Current recommendations on lipid lowering treatment in diabetes with chronic kidney disease [51].

CKD stage/risk category  Treatment  LDL cholesterol goal 
EAS/ESC, 2021  Very high >G3b or G3aA2 or A3 High intensity statin (Class IA) ± ezetimibe (Class IB) / PCSK9 inhibitor (Class IIbC) Step 1: <1.8 mmol/l and 50% reduction from baseline
Step 2: <1.4 mmol/l* (if established ASCVD Class IA, if not IIbC)

ASCVD: atherosclerotic cardiovascular disease; LDL: low-density lipoprotein

*Based on residual 10-year cardiovascular risk, lifetime cardiovascular risk and treatment benefit, comorbidities, frailty and patient preferences.

Class IA (recommended, high evidence), IB (recommended, moderate evidence), IIbC (may be considered, low evidence).

Complications of chronic kidney disease


References for this section: [59–65] 

Diabetes mellitus, chronic kidney disease and treatment with blockers of the renin-angiotensin-aldosterone system (RAAS) are major risk factors for hyperkalaemia. For this reason, patients with diabetic kidney disease are at high risk of hyperkalaemia. Up to now, there are no clinical trials studying relevant clinical outcomes in patients with diabetic kidney disease and chronic hyperkalaemia. Novel molecules are or will soon be available for potassium control in chronic kidney disease, and are briefly discussed here. The recommendations are not specific to diabetic kidney disease.

General recommendations

Figure 4 Treatment of acute hyperkalaemia. Suggested management algorithm for acute hyperkalaemia in adult patients (adapted from: Clase CM, et al. Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2020;97(1):42–61 [59]). Depending on the patient and the clinical situation, the sequence of procedures may be adapted.

Treatment of chronic hyperkalaemia

Mild to moderate stable hyperkalaemia (4.5–6 mmol/l) 

Severe hyperkalaemia (>6 mmol/l) 

Table 7Potassium binders (modified from [61–63]).

Polystyrene sulphonate (Resonium®)  Patiromer (Veltassa®)  SZC (sodium zirconium cyclosilicate) 
Approval in Switzerland Yes Yes* No
Formulation Dissolvable powder Dissolvable powder
Application Oral or rectal Oral Oral
Counterion Sodium Calcium Sodium
Cations bound K+, Mg2+, Ca2+  K+, Mg2+  K+ 
Chemical properties Polymer; sodium salt of polystyrene sulphonic acid Polymer; patiromer sorbitex calcium Non-polymer; non-absorbed zirconium silicate
Mechanism of action Exchanges Na+ for K+, Mg2+, Ca2+  Exchanges Ca2+ for K+; also binds Mg2+  Captures K+ in exchange for hydrogen and Na+ 
Counterion content Na+: 100 mg/g SPS Ca2+: 191 mg/g patiromer Na+: 80 mg/g SZC
Site of action Colon/rectum Distal colon Entire GI tract
Onset of action 1–2 h 4–7 h 1 h
interactions Lithium, levothyroxin edigitalis, sorbitol Reduced systemic exposure of coadministered ciprofloxacin, metformin, and levothyroxine. No interaction when patiromer and these drugs were taken 3 h apart No significant drug-drug interactions
Separate from oral medications by at least 3 h before or 3 h after; if gastroparesis, separate other medications by 6 h Take other oral medications at least 3 h before or 3 h after administration Take other oral medications with gastric pH-dependent availability at least 2 h before or 2 h after
Side effects GI: nausea, vomiting, diarrhoea, constipation. Serious GI effects: ileus, intestinal ulcer/necrosis, perforation, haemorrhage, ischaemic colitis. Electrolyte disturbance: hypokalaemia, hypocalcaemia, hypomagnesaemia, oedema and hypertension due to sodium retentionH Hypomagnesaemia and hypokalaemia; diarrhaea, constipation, nausea, flatulence, abdominal discomfort; potentially calcium overloading Hypokalaemia, Oedema
Setting Acute hyperkalaemia Chronic hyperkalaemia Acute and chronic hyperkalaemia
Dosage 15–60 g (1–4×/d); Rectal: 30–50 g (1–4×/d) Initial: 8.4 g qd (max.: 25.2 g orally once daily ); dose can be increased by 8.4 g increments at one week intervals Initial: 10 g orally 3 times daily for 48 h
Maintenance dose 15–60 g once daily 8.4–25.2g once daily 10 g
Cost + +++

* Veltassa® is reimbursed by the health insurance company after consultation with the doctor in charge for adult, non-dialysed patients with CKD (treatment must be started in CKD stage G3 or 4; the glomerular filtration rate must be below 60 ml/min/1.73 m2), who developed chronic recurrent hyperkalemia during therapy with an inhibitor of the renin-angiotensin-aldosterone system, as determined by repeated measurements, and for whom cation exchange resins must be used because the non-drug measures (diet) and the previous drug measures (e.g. potassium-lowering diuretics) were not sufficient to normalize potassium levels (below 5.5 mmol/l). The initial prescription of Veltassa® can only be made by a nephrologist or cardiologists.

Management of RAAS blocker therapy in patients at risk for hyperkalaemia


References for this section: [66–72] 

Anaemia is a common complication of all types of renal disease, occurring usually in advanced stages. Its pathophysiology is multifactorial, involving deficient erythropoietin production, decreased iron availability and inflammation among others. In patients with type 2 diabetes and chronic kidney disease, anaemia is associated with an increased risk of renal and cardiovascular events. Anaemia is also associated with increased mortality and a higher risk for hospitalisation in chronic kidney disease.

There are no specific recommendations for the management of anaemia in diabetic kidney disease as compared to nondiabetic kidney diseases; therefore, anaemia guidelines for chronic kidney disease apply (KDIGO anaemia guidelines).

Definition of anaemia: <12 g/dl in females, <13 g/dl in males.

Frequency of anaemia monitoring:



Iron therapy in anaemic patients:

ESA use in anaemic patients 

In dialysis and nondialysis patients with chronic kidney disease, several studies have shown that targeting haemoglobin levels ≥13 g/dl increases the risk of adverse outcomes. The TREAT trial was a randomised, double-blind, placebo-controlled study in 4000 nondialysis diabetic patients with chronic kidney disease. Half received darbepoetin alfa to target a haemoglobin level of 13 g/dl, while the other half received placebo and were treated with an ESA only if their hemoglobin fell below 9 g/dl. The group with the higher haemoglobin concentration showed a significant reduction in the need for blood transfusions, but at best a marginal improvement in quality of life. TREAT failed to show a beneficial effect of higher haemoglobin on hard cardiovascular or renal endpoints. In contrast, the risk of venous and arterial thromboembolism increased significantly in the high haemoglobin group, and the risk of stroke was almost double in patients in the higher haemoglobin arm. In the group of patients who had malignant disease at baseline, the number of cancer-related deaths was increased more than tenfold in the higher haemoglobin group.

Chronic kidney disease-mineral and bone disorder

 References for this section: [73–75] 

Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a universal complication of progressive loss of kidney function. Biochemical abnormalities, vascular calcification and bone fragility constitute the CKD-MBD syndrome. CKD-MBD is associated with increased risks for morbidity and mortality in observational studies.

For diabetic kidney disease, there are no specific guidelines and recommendations for the management of CKD-MBD. The proposed recommendations reflect guidelines for chronic kidney disease irrespective of aetiology.

Laboratory tests for CKD-MBD

The frequency of laboratory tests should consider chronic kidney disease stage and progression, and individual factors to monitor trends and treatment efficacy.

CKD KDIGO stage G3a–G3b:

CKD KDIGO stage G4:

CKD KDIGO stage G5, including G5D:

Assessing vascular calcifications

For chronic kidney disease stage G3a–G5D vascular calcifications should be assessed in an individual approach to detect patients at the highest risk for cardiovascular events.

Assessing osteoporosis / renal osteodystrophy

This topic should be managed by an experienced nephrologist as inadequate therapy may do more harm than good. Patients with diabetes and chronic kidney disease are at increased risk for osteoporosis and renal osteodystrophy. Importantly, osteoporosis and renal osteodystrophy are distinct disorders. Their prevalence depends on the disease stage. Osteoporosis can be present alone or in combination with renal osteodystrophy (fig. 5).

Figure 5 Osteoporosis and osteodystrophy in chronic kidney disease (CKD).

The term “renal osteodystrophy” is used to describe alterations in bone morphology connected to chronic kidney disease detected on bone biopsy. It is classified into five distinct forms, which can overlap: osteitis fibrosa, mild hyperparathyroidism, osteomalacia, adynamic bone disease, and mixed uraemic osteodystrophy.

Therapy for CKD-MBD: dietary interventions and drugs

Chronic metabolic acidosis

References for this section: [76–78] 

Metabolic acidosis is characterised by a serum bicarbonate level <22 mmol/l in an individual with normal pulmonary function. It is common in chronic kidney disease and represents an independent and modifiable risk factor for progression of the disease. Importantly, even before frank metabolic acidosis occurs, multiple adaptive responses that increase acid excretion are activated. They include activation of pathways, such as the intrakidney RAAS, that mediate the immediate benefit of increased acid excretion, but chronically become maladaptive and promote a decline in kidney function. Importantly, patients with diabetic kidney disease are at increased risk for type IV renal tubular acidosis, with or without hyperkalaemia, caused by hyporeninaemic hypoaldosteronism.

For diabetic kidney disease and chronic metabolic acidosis, there are no specific guidelines. The proposed recommendations reflect current guidelines for chronic kidney disease irrespective of aetiology. This section does not discuss acute metabolic acidosis secondary to SGLT2 inhibitors (euglycaemic ketoacidosis) or metformin (lactic acidosis).

Assessing metabolic acidosis in CKD

Overt metabolic acidosis commonly develops if GFR declines below 40 ml/min/1.73 m2. Importantly, in individuals with diabetic kidney disease it may manifest earlier due to type IV RTA, which has to be suspected in patients with hyperkalaemia.

Venous blood gas analysis is sufficient to measure bicarbonate concentration.

Suggested monitoring: 

CKD KDIGO stage G3a–G3b:

CKD KDIGO stage G4: 

CKD KDIGO stage G5, including G5D:

In patients receiving treatments for acidosis or with biochemical abnormalities:

Prevention and therapy of metabolic acidosis: dietary interventions and oral alkali supplements 

End-stage renal disease

Blood glucose control in haemodialysis patients

References for this section: [79–84] 

There is an increasing prevalence of diabetes in haemodialysis centres, reaching 30–45% of patients. These patients have variable clinical outcomes and life expectancy. On average, the 5-year mortality of patients with diabetes on haemodialysis is over 50%. Goals of glucose control should be individualised to the patient’s prognosis. Among patients with more stringent goals such as those on the transplantation list, basal bolus therapy is often proposed with 24-hour glucose monitoring.


Monitoring glycaemic control

Goals of therapy in haemodialysis

Antidiabetic therapy in haemodialysis patients

See figure 2 for therapies indicated in end-stage renal disease.


Continuous glucose monitoring devices in haemodialysis patients

Continuous glucose monitoring has become the standard of care in patients at high risk of hypoglycaemia and on intensive insulin regimens. However, fluid shifts between interstitial and intravascular spaces that occur during dialysis sessions, uraemia and acidosis have the potential to impact the performance of commercially available continuous glucose monitoring devices. Non-therapeutic continuous glucose monitoring for a short period in both haemodialysis and peritoneal dialysis was shown to improve glycaemic control thanks to more frequent treatment adaptations. There are ongoing studies examining the effectiveness of therapeutic continuous glucose monitoring devices with haemodialysis.

Although not all continuous glucose monitoring sensors are validated for haemodialysis, their use outside haemodialysis sessions is highly recommended. With the approval of the patient, the data collected in a cloud can be viewed at all times by healthcare providers. We review the advantages and disadvantages of systems for haemodialysis.

Flash system Freestyle Libre  

CGMS Dexcom G6 

CGMS Guardian Connect  

Implantable sensor Eversense 

Prevention of hypoglycaemia in haemodialysis patients

Blood glucose control in peritoneal dialysis patients

References for this section: [85–96] 


Modalities of peritoneal dialysis

Peritoneal dialysis solutions (dialysates)

Effects of peritoneal dialysis on glycaemic control

Methods of monitoring glycaemic control

Glycated haemoglobin (HbA1c):

Self-monitoring of blood glucose: 

Since icodextrin results in elevated blood levels of maltose, only glucose-specific monitors and test strips that utilise the enzyme glucose dehydrogenase must be used. Pyrroloquinolinequinone (GDH-PQQ) or glucose-dye-oxidoreductase test strips are contraindicated because they will give falsely elevated readings leading to insulin misuse and hypoglycaemia events. New test strips have been designed to minimise interference with non-glucose sugars and most glucometers in Switzerland are compatible. Companies providing dialysates have the information on interferences with glucometers.

Continuous glucose monitoring: 

Data on the accuracy of therapeutic continuous glucose monitoring in the setting of peritoneal dialysis are still not available.

Suggested antidiabetic treatment regimens for patients on peritoneal dialysis

Indications and contraindications are similar to those discussed in haemodialysis (see above). The main difference relies on the use of antidiabetic drugs to prevent glucose fluctuations induced by peritoneal dialysis solutions. In this respect, insulin regimens offer the most adjustable therapies with a range of duration of action (from 1.5 to 48 hours). Timing of insulin action should take into account the abrupt onset of glucose diffusion at start of dialysis and the abrupt stop when glucose solution is drained.

In most patients on insulin therapy at initiation of peritoneal dialysis, insulin dosages should be increased especially in those receiving hypertonic exchanges. One study showed that diabetic patients receiving a standard 6 l/day dialysis exchange, had a 27% increase in insulin requirements.

Kidney transplantation

References for this section: [97–106] 

Solid organ transplantation is an established and routine therapeutic option that has transformed the survival and quality of life of patients with end-organ dysfunction. Post-transplant diabetes mellitus (PTDM), also known as new-onset diabetes after transplantation, is a common and important complication following solid organ transplantation. PTDM in kidney transplant patients is associated with decreased patient and graft survival and other adverse outcomes including increased cardiovascular risk, infection and graft rejection. The reported incidence of PTDM varies from 4% to 25% of kidney transplant recipients. Approximately 50% of kidney transplant recipients need antidiabetic therapy (including pre-existing diabetes and PTDM).

Risk factors for PTDM

Table 8Risk of post-transplantation diabetes mellitus with different medications.

Medication  Risk of post-transplantation diabetes mellitus 
Corticosteroids Increased
Tacrolimus Increased
Ciclosporin Slightly increased
mTOR ihibitor Increased
Mycophenolic acid Not diabetogenic
Azathioprine Not diabetogenic
Belatacept Not diabetogenic
Basiliximab Probably increased
Thymoglobulin Not diabetogenic

Pretransplant baseline evaluation

Early hyperglycaemia after transplantation

Diagnosis of PTDM

A diagnosis of PTDM is valid in patients on a stable immunosuppressive regimen, in the absence of infection, and at least 46 days after transplantation. Although the criteria for PTDM are based on criteria for diabetes in the general population, it is unclear whether thresholds for diabetes risk are the same. Some data suggest that criteria for prediabetes and diabetes are all associated with mortality risk in kidney transplant patients.

Prevention and management of early post-transplantation hyperglycaemia and PTDM

Non-pharmacological preventive and management strategies

Antidiabetic therapies

Modification of immunosuppression

Glycaemic targets in PTDM

Encourage self-monitoring of glucose early after transplantation.

Life-style management and nutrition

References for this section: [107–111] 

Life-style management including individualised nutrition therapy, physical activity and interventions for smoking cessation are cornerstones of diabetes management and cardiovascular disease risk reduction and should be reinforced at any time during the course of diabetes and diabetic kidney disease.

In overweight patients with mild to moderate chronic kidney disease, therapies favouring weight loss as treatment with GLP1 receptor agonists or SGLT2 inhibitors and lifestyle changes reinforced by programmes such as Diafit in Switzerland are highly encouraged. However, in more advanced disease (eGFR <30 ml/min/1.73 m2), weight loss may lead to muscle wasting and worse outcomes.

Living with diabetes and chronic kidney disease is a huge challenge for dietary adjustments. The combination of these two conditions makes diet more complicated, as restrictions required by the renal diet may conflict with previous dietary recommendations for diabetes. Successful dietary management requires careful planning, regular assessment of nutritional status and of laboratory values. Poor adherence to the diet puts patients at risk for acute complications such as fluid overload, hyperkalaemia, hyperphosphataemia as well as worsening kidney disease. Diet interventions are recommended to improve adherence to diet and to prevent muscle wasting, sarcopenia and cachexia, which contribute to frailty and morbidity. Early, individualised counselling and nutritional intervention in recently hospitalised patients with chronic kidney disease at nutritional risk are highly recommended with the recent demonstration of decreased mortality and complications at 30 days.

Details of dietary interventions are beyond the scope of these recommendations. All recommendations need to be adapted individually.

The general dietary approach we propose is as follows:


More than 30% of people with diabetes mellitus develop chronic kidney disease. A considerable number of them progress to kidney failure requiring dialysis or transplantation. Hence, there is a great need for efficient evidence-based management of these patients to minimise negative outcomes. Our guidelines address the relevant aspects and provide recommendations for the treatment of diabetic kidney disease and its complications. We also provide advice on screening for and establishing the diagnosis of chronic kidney disease in individuals with type 2 diabetes. Where evidence for diabetic kidney disease is lacking, we have integrated the current recommendations for chronic kidney disease in general.

Developments in recent years have brought effective new therapeutic options such as SGLT2 inhibitors and GLP1 receptor agonists which slow the progression of diabetic kidney disease and/or significantly lower the risk of cardiovascular complications.

Figure 6 Interventions to slow DKD progression and/or reduce cardiovascular disease (adapted from: Shlipak MG, et al. The case for early identification and intervention of chronic kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2021;99:34–47 [112]).

RAS blockade, SGLT2i and GLP1Ra use in more advanced CKD to be considered individually and based on drug label and figure 2.

҂ No statin initiation in dialysis.

* RAS blockers and SGLT2i slow eGFR decline in albuminuria stage A3.

# SGLT2i and GLP1Ra decrease renal and cardiovascular morbidity in high CV risk patients.

§ Cardiovascular and renal protection with finerenone in albuminuria stage A2 and A3.

Fortunately, the field of diabetic kidney diseases is still rapidly evolving. Several clinical trials of novel agents targeting different pathways in patients with diabetes mellitus are underway. New substances such as nonsteroidal mineralocorticoid receptor antagonists decrease renal and cardiovascular risk in patients with diabetic kidney disease. Endothelin antagonists are in the therapeutic pipeline. These new therapies might be combined with currently available drugs in the future such that an individualised approach can be accomplished. Due to the dynamic development, we plan to publish the guidelines on an electronic platform, so that they can be updated promptly in case of clinically relevant new findings. We are optimistic that our guidelines will significantly contribute to a high-quality multidisciplinary care of patients with diabetic kidney disease in Switzerland in the future.


We thank the SSN and SSED committees for carefully reviewing the document and bringing valuable suggestions.


Disclosure statement

All authors have completed and submitted the International Committee of Medical Journal Editors form for disclosure of potential conflicts of interest. SdS participated to advisory boards for Astra Zeneca, Otsuka and Astellas. AZ has participated to advisory boards for NovoNordisk, Bayer, Astra Zeneca, Mundipharma and Boehringher Ingelheim. CC, FL and BV have no conflict of interest. HS participated in advisory boards for Mundipharma, Astra Zeneca, Vifor, Bayer, Astellas and Amgen. AJ has participated to advisory boards for Mundipharma Medical. SB has received advisory board honoraria and speaker fees from Novonordisk, Sanofi, Amgen, Daiichi-Sankyo, Novartis, Boehringer, Bayer, AstraZeneca. No other potential conflict of interest was disclosed.

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