We report a rare case of the concurrent manifestation of central diabetes insipidus (CDI) and type 2 diabetes mellitus (DM). A 56 year-old man was diagnosed as a type 2 DM on the basis of hyperglycemia with polyuria and polydipsia at a local clinic two months ago and started an oral hypoglycemic medication, but resulted in no symptomatic improvement at all. Upon admission to the university hospital, the patient`s initial fasting blood sugar level was 140mg/dL, and he showed polydipsic and polyuric conditions more than 8 L urine/day. Despite the hyperglycemia controlled with metformin and diet, his symptoms persisted. Further investigations including water deprivation test confirmed the coexisting CDI of unknown origin, and the patient`s symptoms including an intense thirst were markedly improved by desmopressin nasal spray (10 μg/day). The possibility of a common origin of CDI and type 2 DM is raised in a review of the few relevant adult cases in the literature.

We report a rare case of the concurrent manifestation of central diabetes insipidus (CDI) and type 2 diabetes mellitus (DM). A 56 year-old man was diagnosed as a type 2 DM on the basis of hyperglycemia with polyuria and polydipsia at a local clinic two months ago and started an oral hypoglycemic medication, but resulted in no symptomatic improvement at all. Upon admission to the university hospital, the patient`s initial fasting blood sugar level was 140mg/dL, and he showed polydipsic and polyuric conditions more than 8 L urine/day. Despite the hyperglycemia controlled with metformin and diet, his symptoms persisted. Further investigations including water deprivation test confirmed the coexisting CDI of unknown origin, and the patient`s symptoms including an intense thirst were markedly improved by desmopressin nasal spray (10 μg/day). The possibility of a common origin of CDI and type 2 DM is raised in a review of the few relevant adult cases in the literature.

Recognizing the underlying causes of hypokalemic paralysis seems to be essential for the appropriate management of affected patients and their prevention ofrecurrent attacks. There is, however, a paucity of documented reports on the etiology of hypokalemic paralysis in Korea. We retrospectively analyzed 34 patients with acute flaccid weakness due to hypokalaemia who were admitted during the 5-year study period in order to determine the spectrum of hypokalemic paralysis in Korea and to identify the differences in clinical parameters all across the causes of hypokalemic paralysis. We divided those 34 patients into 3 groups; the 1st group, idiopathic hypokalemic periodic paralysis (HPP), the 2nd, thyrotoxic periodic paralysis (TPP), and the 3rd group, secondary hypokalemic paralysis (HP) without TPP. Seven of the patients (20.6%) were diagnosed as idiopathic HPP considered the sporadic form, and 27 patients (79.4%) as secondary HP. Among the patients diagnosed as secondary HP, 16 patients (47.1%) had TPP. Patients of secondary hypokalemic paralysis without TPP required a longer recovery time compared with those who had either idiopathic HPP or TPP. This is due to the fact that patients of secondary HP had a significantly negative total body potassium balance, whereas idiopathic HPP and TPP were only associated with intracellular shift of potassium. Most of the TPP patients included in our study had overt thyrotoxicosis while 3 patients had subclinical thyrotoxicosis. This study shows that TPP is the most common cause of hypokalemic paralysis in Korea. And we suggest that doctors should consider the presence of TPP in patients of hypokalemic paralysis even if they clinically appear to be euthyroid state.

Cardio-renal syndrome (CRS) is a frequent and life-threatening syndrome. It is a disorder of the heart and kidneys in which acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Acute kidney injury (AKI) is strongly associated with increased morbidity and mortality in patients with CRS. Early detection of renal dysfunction is not possible using the traditional marker, serum creatinine, and therefore efforts to explore possible biomarkers for early detection of AKI are being made. Apart from predicting AKI, several biomarker studies also identified predictors for poor prognosis such as the need for renal replacement therapy (RRT) or death. It is possible that biomarkers can become risk factors in an improvement of clinical outcomes of CRS. Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in patients with renal dysfunction and the treatment for this disease can be modified based on cardiac biomarkers. In addition to natriuretic peptides, which are established cardiac markers, several new biomarkers have been identified and may play important roles in CRS. In this review, we will briefly summarize the literature on novel renal and cardiac biomarkers and discuss their potential roles in the clinical outcome of CRS.

Atomic force microscopy (AFM) has become an important medical and biological tool for non-invasive imaging and measuring the mechanical changes of cells since its invention by Binnig et al. AFM can be used to investigate the mechanical properties of cellular events in individual living cells on a nanoscale level. In addition, the dynamic cellular movements induced by biochemical activation of specific materials can be detected in real time with three dimensional resolution. Force measurement with the use of AFM has become the tool of choice to monitor the mechanical changes of variable cellular events. In addition, the AFM approach can be applied to measure cellular adhesion properties. Moreover, the information gathered from AFM is important to understanding the mechanisms related to cellular movement and mechanical regulation. This review will discuss recent contributions of AFM to cellular physiology with a focus on monitoring the effects of antihypertensive agents in kidney cells.

Sodium is the principal solute in the extracellular compartment and the major component of serum osmolality. In normal persons in the steady state, sodium homeostasis is achieved by a balance between the dietary intake and the urinary output of sodium, whereas in intermittent hemodialysis patients, sodium balance depends on dietary intake and sodium removal during hemodialysis. Thus, the main goal of hemodialysis is to remove precisely the amount of sodium that has accumulated during the interdialytic period. Sodium removal during hemodialysis occurs via convective (~78%) and diffusive losses (~22%) between dialysate and plasma sodium concentration. The latter (the sodium gradient) is an important factor in the ``fine tuning`` of sodium balance during intermittent hemodialysis. Most use fixed dialysate sodium concentrations, but each patient has his/her own plasma sodium concentrations pre-hemodialysis, which are quite reproducible and stable in the long-term. Thus, in many patients, a fixed dialysate sodium concentration will cause a persistent positive sodium balance during dialysis, which could possibly cause increased thirst, interdialytic weight gain, and mortality. Several methods will be discussed to reduce positive sodium balance, including sodium alignment.