The following characteristics suggest the possibility of a diagnosis of MODY in hyperglycemic and diabetic patients:

- Mild to moderate hyperglycemia (typically 130–250 mg/dl, or 7–14 mmol/l) discovered before 30 years of age. However, anyone under 50 can develop MODY.

- A first-degree relative with a similar degree of diabetes.

- Absence of positive antibodies or other autoimmunity (e.g., thyroiditis) in patient and family. However, Urbanova et al. found that about one quarter of Central European MODY patients are positive for islet cell autoantibodies (GADA and IA2A). Their expression is transient but highly prevalent. The autoantibodies were found in patients with delayed diabetes onset, and in times of insufficient diabetes control. The islet cell autoantibodies are absent in MODY in at least some populations (Japanese, Britons).

- Persistence of a low insulin requirement (e.g., less than 0.5 u/kg/day) past the usual "honeymoon" period.

- Absence of obesity (although overweight or obese people can get MODY) or other problems associated with type 2 diabetes or metabolic syndrome (e.g., hypertension, hyperlipidemia, polycystic ovary syndrome).

- Insulin resistance very rarely happens.

- Cystic kidney disease in patient or close relatives.

- Non-transient neonatal diabetes, or apparent type 1 diabetes with onset before six months of age.

- Liver adenoma or hepatocellular carcinoma in MODY type 3

- Renal cysts, rudimentary or bicornuate uterus, vaginal aplasia, absence of the vas deferens, epidymal cysts in MODY type 5

The diagnosis of MODY is confirmed by specific gene testing available through commercial laboratories.

Currently, MODY is the final diagnosis in 1%–2% of people initially diagnosed with diabetes. The prevalence is 70–110 per million population. 50% of first-degree relatives will inherit the same mutation, giving them a greater than 95% lifetime risk of developing MODY themselves. For this reason, correct diagnosis of this condition is important. Typically patients present with a strong family history of diabetes (any type) and the onset of symptoms is in the second to fifth decade.

There are two general types of clinical presentation.

- Some forms of MODY produce significant hyperglycemia and the typical signs and symptoms of diabetes: increased thirst and urination (polydipsia and polyuria).

- In contrast, many people with MODY have no signs or symptoms and are diagnosed either by accident, when a high glucose is discovered during testing for other reasons, or screening of relatives of a person discovered to have diabetes. Discovery of mild hyperglycemia during a routine glucose tolerance test for pregnancy is particularly characteristic.

MODY cases may make up as many as 5% of presumed type 1 and type 2 diabetes cases in a large clinic population. While the goals of diabetes management are the same no matter what type, there are two primary advantages of confirming a diagnosis of MODY.

- Insulin may not be necessary and it may be possible to switch a person from insulin injections to oral agents without loss of glycemic control.

- It may prompt screening of relatives and so help identify other cases in family members.

As it occurs infrequently, many cases of MODY are initially assumed to be more common forms of diabetes: type 1 if the patient is young and not overweight, type 2 if the patient is overweight, or gestational diabetes if the patient is pregnant. Standard diabetes treatments (insulin for type 1 and gestational diabetes, and oral hypoglycemic agents for type 2) are often initiated before the doctor suspects a more unusual form of diabetes.

The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss. Other symptoms that are commonly present at diagnosis include a history of blurred vision, itchiness, peripheral neuropathy, recurrent vaginal infections, and fatigue. Many people, however, have no symptoms during the first few years and are diagnosed on routine testing. A small number of people with type 2 diabetes mellitus can develop a hyperosmolar hyperglycemic state (a condition of very high blood sugar associated with a decreased level of consciousness and low blood pressure).

MODY 3 is a form of maturity onset diabetes of the young.

MODY 3 (also known as HNF1A-MODY) is caused by mutations of the HNF1-alpha; gene, a homeobox gene on chromosome 12. This is the most common type of MODY in populations with European ancestry, accounting for about 70% of all cases in Europe. HNF1α is a transcription factor (also known as transcription factor 1, TCF1) that is thought to control a regulatory network (including, among other genes, HNF1α) important for differentiation of beta cells. Mutations of this gene lead to reduced beta cell mass or impaired function. MODY 1 and MODY 3 diabetes are clinically similar. About 70% of people develop this type of diabetes by age 25 years, but it occurs at much later ages in a few. This type of diabetes can often be treated with sulfonylureas with excellent results for decades. However, the loss of insulin secretory capacity is slowly progressive and most eventually need insulin.

This is the form of MODY which can most resemble ordinary type 1 diabetes, and one of the incentives for diagnosing it is that insulin may be discontinued or deferred in favor of oral sulfonylureas. Some people treated with insulin for years due to a presumption of type 1 diabetes have been able to switch to pills and discontinue injections. Long-term diabetic complications can occur if the glucose is not adequately controlled.

High-sensitivity measurements of CRP may help to distinguish between HNF1A-MODY and other forms of diabetes

Type 2 diabetes is typically a chronic disease associated with a ten-year-shorter life expectancy. This is partly due to a number of complications with which it is associated, including: two to four times the risk of cardiovascular disease, including ischemic heart disease and stroke; a 20-fold increase in lower limb amputations, and increased rates of hospitalizations. In the developed world, and increasingly elsewhere, type 2 diabetes is the largest cause of nontraumatic blindness and kidney failure. It has also been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia. Other complications include acanthosis nigricans, sexual dysfunction, and frequent infections.

"Common symptoms of NDM includes:"

- Thirst and Frequent Urination

An excessive thirst (also known as polydipsia) and increased urination (also known as polyuria) are common signs of diabetes. An individual with diabetes, have accumulated blood glucose. Their kidneys are working overtime to filter and uptake excess sugar. However, their kidneys cannot keep up, excess sugar is excreted into their urine, and this drag along fluids from the diabetic's tissues. This may lead to more frequent urination and lead to dehydration. As a diabetic individual drinks more fluids to satisfy their thirst, he or she urinates even more.

- Dehydration

Effected areas of the body are the eyes, mouth, kidneys, heart, and pancreas. Other symptoms of dehydration includes headache, thirst and dry mouth, dizziness, tiredness, and dark colored urine. In severe cases of dehydration in diabetics, low blood pressure, sunken eyes, a weak pulse or rapid heart beat, feeling confused or fatigue. Dehydration and high blood glucose for extended period of time, the diabetic's kidney would try to filter the blood of access glucose and excrete this as urine. As the kidneys are filtering the blood, water is being removed from the blood and would need to be replaced. This leads to an increased thirst when the blood glucose is elevated in a diabetic individual. Water is needed to re-hydrate the body. Therefore, the body would take available from other parts of the body, such as saliva, tears, and from cells of the body. If access water is not available, the body would not be able to pass excess glucose out of the blood by urine and can lead to further dehydration.

"Severe symptoms of NDM (Deficiency of insulin):"

- Ketoacidosis

Is a diabetic complication that occurs when the body produces high levels of acid in the blood (ketones). This effects the pancreas, fat cells, and kidneys. This condition occurs when the body cannot produce enough insulin. In the absence or lack of insulin, the body of an diabetic individual will break down fat as fuel. This process produces a buildup of acids in the bloodstream known as ketones, in which leads to ketoacidosis if left untreated. The symptoms of ketoacidosis develop rapidly or within 24 hours. Symptoms of ketoacidosis are excessive thirst, frequent urination, nausea or vomiting, stomach pain, tiredness, shortness or fruity smell on breath and confusion.

- Intrauterine Growth Restriction

A condition in which the unborn baby is smaller than he or she should be, due to the fact he or she not growing at a normal rate in the womb. Delayed growth puts the baby at risk of certain problems during pregnancy, delivery, and after birth. The problems are as follows: baby's birth weight is 90% less than normal weight, difficulty handling vaginal delivery, decreased oxygen levels, hypoglycemia (low blood glucose), low resistance to infection, low Apgar scores (a test given after birth to test the baby's physical condition and evaluate if special medical care is needed), Meconium aspiration (inhaling of stools passed while in the uterus) which causes breathing issues, irregular body temperature and high red blood cell count.

- Hyperglycemia

A condition characterized as high blood glucose, which occurs when the body has too little insulin or when the body cannot use insulin properly. Hyperglycemia affects the pancreas, kidneys, and body's tissues. Characterization of hyperglycemia is high blood glucose, high levels of sugar in the urine, frequent urination and increase thirst.

- Hypoglycemia

A condition characterized an extremely low blood glucose, usually less than 70 mg/dL. Areas of the body that are affected, pancreas, kidneys, and mental state.

The classic symptoms of untreated diabetes are weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 DM, while they usually develop much more slowly and may be subtle or absent in type 2 DM.

Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known ones above, they include blurry vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.

Low blood sugar is common in persons with type 1 and type 2 DM. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious issues such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and (rarely) permanent brain damage or death in severe cases. Moderate hypoglycemia may easily be mistaken for drunkenness; rapid breathing and sweating, cold, pale skin are characteristic of hypoglycemia but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.

People (usually with type 1 DM) may also experience episodes of diabetic ketoacidosis, a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness.

A rare but equally severe possibility is hyperosmolar hyperglycemic state, which is more common in type 2 DM and is mainly the result of dehydration.

Gestational diabetes is formally defined as "any degree of glucose intolerance with onset or first recognition during pregnancy". This definition acknowledges the possibility that a woman may have previously undiagnosed diabetes mellitus, or may have developed diabetes coincidentally with pregnancy. Whether symptoms subside after pregnancy is also irrelevant to the diagnosis.

A woman is diagnosed with gestational diabetes when glucose intolerance continues beyond 24–28 weeks of gestation.

The White classification, named after Priscilla White, who pioneered research on the effect of diabetes types on perinatal outcome, is widely used to assess maternal and fetal risk. It distinguishes between gestational diabetes (type A) and pregestational diabetes (diabetes that existed prior to pregnancy). These two groups are further subdivided according to their associated risks and management.

The two subtypes of gestational diabetes under this classification system are:

- Type A1: abnormal oral glucose tolerance test (OGTT), but normal blood glucose levels during fasting and two hours after meals; diet modification is sufficient to control glucose levels

- Type A2: abnormal OGTT compounded by abnormal glucose levels during fasting and/or after meals; additional therapy with insulin or other medications is required

Diabetes which existed prior to pregnancy is also split up into several subtypes under this system:

- Type B: onset at age 20 or older and duration of less than 10 years.

- Type C: onset at age 10–19 or duration of 10–19 years.

- Type D: onset before age 10 or duration greater than 20 years.

- Type E: overt diabetes mellitus with calcified pelvic vessels.

- Type F: diabetic nephropathy.

- Type R: proliferative retinopathy.

- Type RF: retinopathy and nephropathy.

- Type H: ischemic heart disease.

- Type T: prior kidney transplant.

An early age of onset or long-standing disease comes with greater risks, hence the first three subtypes.

Two other sets of criteria are available for diagnosis of gestational diabetes, both based on blood-sugar levels.

Criteria for diagnosis of gestational diabetes, using the 100 gram Glucose Tolerance Test, according to Carpenter and Coustan:

- Fasting 95 mg/dl

- 1 hour 180 mg/dl

- 2 hours 155 mg/dl

- 3 hours 140 mg/dl

Criteria for diagnosis of gestational diabetes according to National Diabetes Data Group:

- Fasting 105 mg/dl

- 1 hour 190 mg/dl

- 2 hours 165 mg/dl

- 3 hours 145 mg/dl

Neonatal diabetes mellitus (NDM) is defined as a disease that affects an infant and their body's ability to produce or use insulin. NDM is a monogenic (controlled by a single gene) form of diabetes that occurs in the first 6 months of life. Infants do not produce enough insulin, leading to an increase in . It is a rare disease, occurring in only one in 100,000 to 500,000 live births. NDM can be mistaken for the much more common type 1 diabetes, but type 1 diabetes usually occurs later than the first 6 months of life. There are two types of NDM: permanent neonatal diabetes mellitus (PNDM) is a lifelong condition. Transient neonatal diabetes mellitus (TNDM) is diabetes that disappears during the infant stage but may reappear later in life.

Specific genes that can cause NDM have been identified. The onset of NDM can be caused by abnormal pancreatic development, beta cell dysfunction or accelerated beta cell dysfunction. Individuals with monogenic diabetes can pass it on to their children or future generations. Each gene associated with NDM has a different inheritance pattern.

These depend on poorly understood variations in individual biology and consequently may not be found with all people diagnosed with insulin resistance.

- Increased hunger

- Lethargy (tiredness)

- Brain fogginess and inability to focus

- High blood sugar

- Weight gain, fat storage, difficulty losing weight – for most people, excess weight is from high subcutaneous fat storage; the fat in IR is generally stored in and around abdominal organs in both males and females; it is currently suspected that hormones produced in that fat are a precipitating cause of insulin resistance

- Increased blood cholesterol levels

- Increased blood pressure; many people with hypertension are either diabetic or pre-diabetic and have elevated insulin levels due to insulin resistance; one of insulin's effects is to control arterial wall tension throughout the body

Insulin resistance (IR) is a pathological condition in which cells fail to respond normally to the hormone insulin. The body produces insulin when glucose starts to be released into the bloodstream from the digestion of carbohydrates in the diet. Normally this insulin response triggers glucose being taken into body cells, to be used for energy, and inhibits the body from using fat for energy. The concentration of glucose in the blood decreases as a result, staying within the normal range even when a large amount of carbohydrates is consumed. When the body produces insulin under conditions of insulin resistance, the cells are resistant to the insulin and are unable to use it as effectively, leading to high blood sugar. Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level. This often remains undetected and can contribute to the development of type 2 diabetes or latent autoimmune diabetes of adults. Although this type of chronic insulin resistance is harmful, during acute illness it is actually a well-evolved protective mechanism. Recent investigations have revealed that insulin resistance helps to conserve the brain's glucose supply by preventing muscles from taking up excessive glucose. In theory, insulin resistance should even be strengthened under harsh metabolic conditions such as pregnancy, during which the expanding fetal brain demands more glucose.

People who develop type 2 diabetes usually pass through earlier stages of insulin resistance and prediabetes, although those often go undiagnosed. Insulin resistance is a syndrome (a set of signs and symptoms) resulting from reduced insulin activity; it is also part of a larger constellation of symptoms called the metabolic syndrome.

Insulin resistance may also develop in patients who have recently experienced abdominal or bariatric procedures. This acute form of insulin resistance that may result post-operatively tends to increase over the short term, with sensitivity to insulin typically returning to patients after about five days.

Gestational diabetes is a condition in which a woman without diabetes develops high blood sugar levels during pregnancy. Gestational diabetes generally results in few symptoms; however, it does increase the risk of pre-eclampsia, depression, and requiring a Caesarean section. Babies born to mothers with poorly treated gestational diabetes are at increased risk of being too large, having low blood sugar after birth, and jaundice. If untreated, it can also result in a stillbirth. Long term, children are at higher risk of being overweight and developing type 2 diabetes.

Gestational diabetes is caused by not enough insulin in the setting of insulin resistance. Risk factors include being overweight, previously having gestational diabetes, a family history of type 2 diabetes, and having polycystic ovarian syndrome. Diagnosis is by blood tests. For those at normal risk screening is recommended between 24 and 28 weeks gestation. For those at high risk testing may occur at the first prenatal visit.

Prevention is by maintaining a healthy weight and exercising before pregnancy. Gestational diabetes is a treated with a diabetic diet, exercise, and possibly insulin injections. Most women are able to manage their blood sugar with a diet and exercise. Blood sugar testing among those who are affected is often recommended four times a day. Breastfeeding is recommended as soon as possible after birth.

Gestational diabetes affects 3–9% of pregnancies, depending on the population studied. It is especially common during the last three months of pregnancy. It affects 1% of those under the age of 20 and 13% of those over the age of 44. A number of ethnic groups including Asians, American Indians, Indigenous Australians, and Pacific Islanders are at higher risk. In 90% of people gestational diabetes will resolve after the baby is born. Women, however, are at an increased risk of developing type 2 diabetes.

Hyperproinsulinemia is a disease where insulin is not sufficiently processed before secretion and immature forms of insulin make up the majority of circulating insulin immunoreactivity in both fasting and glucose-stimulated conditions (insulin immunoreactivity refers to all molecules detectable by an insulin antibody, i.e. insulin, proinsulin, and proinsulin-like material). The term is composed of "hyper" - high, "proinsulin" - immature insulin molecule, and "-emia" - blood condition.

Hyperproinsulinemia is more frequent in type 2 diabetes. It has been attributed to either a direct β-cells defect or an indirect effect of cell dysregulation under sustained elevated blood glucose (hyperglycemia).

Some alleles of insulin can cause hyperproinsulinemia (see table 2: monogenic forms of type 1 diabetes, INS (insulin). For a more detailed descriptions of the insulin gene variations leading to hyperproinsulinemia see NCBI's OMIM 176730

The main sign of metabolic syndrome is central obesity (also known as visceral, male-pattern or apple-shaped adiposity), overweight with adipose tissue accumulation particularly around the waist and trunk.

Other signs of metabolic syndrome include high blood pressure, decreased fasting serum HDL cholesterol, elevated fasting serum triglyceride level (VLDL triglyceride), impaired fasting glucose, insulin resistance, or prediabetes.

Associated conditions include hyperuricemia, fatty liver (especially in concurrent obesity) progressing to nonalcoholic fatty liver disease, polycystic ovarian syndrome (in women), erectile dysfunction (in men), and acanthosis nigricans.

High-sensitivity C-reactive protein has been developed and used as a marker to predict coronary vascular diseases in metabolic syndrome, and it was recently used as a predictor for nonalcoholic fatty liver disease (steatohepatitis) in correlation with serum markers that indicated lipid and glucose metabolism. Fatty liver disease and steatohepatitis can be considered as manifestations of metabolic syndrome, indicative of abnormal energy storage as fat in ectopic distribution.

Reproductive disorders (such as polycystic ovary syndrome in women of reproductive age), and erectile dysfunction or decreased total testosterone (low testosterone-binding globulin) in men can be attributed to metabolic syndrome.

Dunnigan-type familial partial lipodystrophy, also known as FPLD Type II and abbreviated as (FPLD2), is a rare monogenic form of insulin resistance characterized by loss of subcutaneous fat from the extremities, trunk, and gluteal region. FPLD recapitulates the main metabolic attributes of the insulin resistance syndrome, including central obesity, hyperinsulinemia, glucose intolerance and diabetes usually type 2, dyslipidemia, hypertension, and early endpoints of atherosclerosis. It can also result in hepatic steatosis. FPLD results from mutations in LMNA gene, which is the gene that encodes nuclear lamins A and C.

Acanthosis nigricans may present with thickened, velvety, relatively darker areas of skin on the neck, armpit and in skin folds.

Acanthosis nigricans is conventionally divided into benign and malignant forms, although may be divided into syndromes according to cause:

- Benign This may include obesity-related, hereditary, and endocrine forms of acanthosis nigricans.

- Malignant. This may include forms that are associated with tumour products and insulin-like activity, or tumour necrosis factor.

An alternate classification system still used to describe acanthosis nigricans was proposed in 1994. It delineates acanthosis nigricans syndromes according to their associated syndromes, including benign and malignant forms, forms associated with obesity and drugs, acral acanthosis nigricans, unilateral acanthosis nigricans, and mixed and syndromic forms.

The primary physiological effect of glucagonoma is an overproduction of the peptide hormone glucagon, which leads to an increase in blood glucose levels through the activation of anabolic and catabolic processes including gluconeogenesis and lipolysis respectively. Gluconeogenesis produces glucose from protein and amino acid materials. It also increases lipolysis, which is the breakdown of fat. The net result is hyperglucagonemia, decreased blood levels of amino acids (hypoaminoacidemia), anemia, diarrhea, and weight loss of 5 to15 kg.

Necrolytic migratory erythema (NME) is a classical symptom observed in patients with glucagonoma and is the presenting problem in 70% of cases. Associated NME is characterized by the spread of erythematous blisters and swelling across areas subject to greater friction and pressure, including the lower abdomen, buttocks, perineum, and groin.

Diabetes mellitus also frequently results from the insulin and glucagon imbalance that occurs in glucagonoma. Diabetes mellitus is present in 80% to 90% of cases of glucagonoma, and is exacerbated by preexisting insulin resistance.

A glucagonoma is a rare tumor of the alpha cells of the pancreas that results in the overproduction of the hormone glucagon. Alpha cell tumors are commonly associated with glucagonoma syndrome, though similar symptoms are present in cases of pseudoglucagonoma syndrome in the absence of a glucagon-secreting tumor.

The onset of symptoms is 5 to 10 years after the disease begins. A usual first symptom is frequent urination at night: nocturia. Other symptoms include tiredness, headaches, a general feeling of illness, nausea, vomiting, frequent daytime urination, lack of appetite, itchy skin, and leg swelling.

Wolcott–Rallison syndrome, WRS, is a rare, autosomal recessive disorder with infancy-onset diabetes mellitus, multiple epiphyseal dysplasia, osteopenia, mental retardation or developmental delay, and hepatic and renal dysfunction as main clinical findings. Patients with WRS have mutations in the EIF2AK3 gene, which encodes the pancreatic eukaryotic translation initiation factor 2-alpha kinase 3.

The principal feature of Laron syndrome is abnormally short stature (dwarfism). Physical symptoms include: prominent forehead, depressed nasal bridge, underdevelopment of mandible, truncal obesity, and micropenis in males. The breasts of females reach normal size, and in some are large in relation to body size. It has been suggested that hyperprolactinemia may contribute to the enlarged breast size. Seizures are frequently seen secondary to hypoglycemia. Some genetic variations decrease intellectual capacity. Laron syndrome patients also do not develop acne, except temporarily during treatment with IGF-1 (if performed).

In 2011, it was reported that people with this syndrome in the Ecuadorian villages are resistant to cancer and diabetes and are somewhat protected against aging. This is consistent with findings in mice with a defective growth hormone receptor gene.

Diabetic nephropathy (diabetic kidney disease) (DN) is the chronic loss of kidney function occurring in those with diabetes mellitus. It is a serious complication, affecting around one-quarter of adult diabetics in the United States. It usually is slowly progressive over years. Pathophysiologic abnormalities in DN begin with long-standing poorly controlled blood glucose levels. This is followed by multiple changes in the filtration units of the kidneys, the nephrons. (There are normally about 3/4-1 1/2 million nephrons in each adult kidney). Initially, there is constriction of the efferent arterioles and dilation of afferent arterioles, with resulting glomerular capillary hypertension and hyperfiltration; this gradually changes to hypofiltration over time. Concurrently, there are changes within the glomerulus itself: these include a thickening of the basement membrane, a widening of the slit membranes of the podocytes, an increase in the number of mesangial cells, and an increase in mesangial matrix. This matrix invades the glomerular capillaries and produces deposits called Kimmelstiel-Wilson nodules. The mesangial cells and matrix can progressively expand and consume the entire glomerulus, shutting off filtration.

The status of DN may be monitored by measuring two values: the amount of protein in the urine - proteinuria; and a blood test called the serum creatinine. The amount of the proteinuria is a reflection of the degree of damage to any still-functioning glomeruli. The value of the serum creatinine can be used to calculate the estimated glomerular filtration rate (eGFR), which reflects the percentage of glomeruli which are no longer filtering the blood.

Treatment with an angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB), which dilates the arteriole exiting the glomerulus, thus reducing the blood pressure within the glomerular capillaries, may delay - but not stop - progression of the disease. Also, three classes of diabetes medications - GLP-1 agonists, DPP-4 inhibitors, and SGLT2 inhibitors - may delay progression.

The proteinuria may become massive, and cause a low serum albumin with resulting generalized body swelling (edema): the nephrotic syndrome. Likewise, the eGFR may progressively fall from a normal of over 90 ml/min/1.73m to less than 15, at which point the patient is said to have end-stage kidney disease (ESKD). Diabetic nephropathy is the most common cause of ESKD, which may require hemodialysis and eventually kidney transplantation to replace the failed kidney function. Diabetic nephropathy is associated with an increased risk of death in general, particularly from cardiovascular disease.