What are the clinical manifestations of diabetes insipidus?

Diabetes insipidus has a typical clinical symptom, which is polyuria. At the same time, the patient will feel thirsty and drink more water. As the disease progresses, the patient's bladder capacity increases due to long-term polyuria, so the frequency of urination will begin to decrease.

1. Hyposonic polyuria

Polyuria is the most prominent symptom in DI patients, while CDI patients generally have an acute onset and a clear date. Urine volume exceeds 2500ml/d or 50ml/(kg.d)], accompanied by thirst and polydipsia. Nocturia increases significantly, and urine volume is generally above 4L/d, rarely exceeding 10L/d, but there are also reports of up to 40L/d. The urine specific gravity is 1.0001-1.0005, and the urine osmotic pressure is 50-200 mOsm/L, which is significantly lower than the plasma osmotic pressure. Long-term polyuria can cause the bladder to hold more urine, so the frequency of urination decreases. Some patients with diabetes insipidus have mild symptoms, with a urine volume of 2.4 to 5 L/d. If water intake is restricted and leads to severe dehydration, the urine specific gravity can reach 1.010 to 1.016, and the urine osmotic pressure can exceed the plasma osmotic pressure by 290 to 600 mOsm/L. If the patient's thirst center is not affected and drinking is not restricted, it will generally only affect sleep and cause physical weakness, but it is not likely to be life-threatening. If the patient's sense of thirst decreases or disappears and water is not replenished in time, it may cause severe water loss, a significant increase in plasma osmotic pressure and serum sodium levels, extreme weakness, fever, mental symptoms, and even death. Once diabetes insipidus is combined with adenohypophysis

2. Clinical manifestations of primary disease

People with secondary diabetes insipidus also have symptoms and signs of the primary disorder. Patients with traumatic CDI may present with transient diabetes insipidus and triphasic diabetes insipidus.

Triphasic diabetes insipidus can be divided into acute phase, intermediate phase and persistent phase. The acute phase is characterized by polyuria, which occurs after injury and generally lasts for 4-5 days. It is mainly because the injury causes neuronal shock, which prevents the release of AVP or releases biologically inactive precursor substances. The intermediate stage is characterized by oliguria and increased urine osmotic pressure, which is caused by the overflow of AVP from degenerated neurons, resulting in a sudden increase in AVP in the circulation. The persistent phase is characterized by persistent polyuria, which occurs at irregular times, with >90% disappearance of magnocellular neurons in the supraoptic nucleus and paraventricular nucleus or >85% irreversible damage to the pituitary stalk.